Current Concepts of Otitis Media and Recent Management Strategies [1 ed.] 9789385999796, 9789351524533

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Current Concepts of Otitis Media and Recent Management Strategies

Current Concepts of Otitis Media and Recent Management Strategies

Editors Anand Job  DLO MS MNAMS Professor Department of ENT-I Christian Medical College Vellore, Tamil Nadu, India

L Paul Emerson  DLO MS (ENT) ENT Consultant Department of ENT-I Christian Medical College Vellore, Tamil Nadu, India

Forewords Mohan Kameswaran Ravi Ramalingam Sunil Chandy

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Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2015, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected] Current Concepts of Otitis Media and Recent Management Strategies First Edition: 2015 ISBN: 978-93-5152-453-3 Printed at

Dedicated to To the memory of my mother Mrs Thanka Job for her love and inspiration My wife Victoria and children Jonathan and Anjana

Contributors Anand Job  DLO MS MNAMS Professor Department of ENT-I Christian Medical College Vellore, Tamil Nadu, India

Shalini Anandan  MD Associate Professor Department of Clinical Microbiology Christian Medical College Vellor, Tamil Nadu, India

John Mathew  DLO MS FRCS Professor Department of ENT Christian Medical College Vellore, Tamil Nadu, India

Swapna Sabastian  MSc PhD Associate Professor Department of ENT Christian Medical College Vellore, Tamil Nadu, India

L Paul Emerson  DLO MS (ENT) ENT Consultant Department of ENT-I Christian Medical College Vellore, Tamil Nadu, India

Foreword It gives me great pleasure in writing the foreword for Current Concepts of Otitis Media and Recent Management Strategies edited and written by Prof Anand Job, Professor of Otolaryngology at venerated Institution, Christian Medical College, Vellore, Tamil Nadu, India. One may wonder, as I did before reading the book, ‘why another book on otitis media?’ The title of the book itself answers the question—the fact of the matter is that otitis media, despite being one of the oldest confounding problems in otolaryngology, continues to throw challenges at the ENT fraternity and like a chameleon changing its colors, keeps changing its character. New knowledge keeps piling up just as new problems arise. Hence, the need for a new update and this book fulfils the need elegantly. The book is complete, comprehensive and cogent. The chapters on biofilms and eosinophilic otitis media are noteworthy in highlighting recent developments. The book is well conceived, thoroughly researched and presented in a simple palatable format. The illustrations add to the contents of the book and do justice to the text. All in all, it’s a very readable and elegant work on the subject. I am sure the book will be of great benefit to ENT practitioners, students of otolaryngology, family physicians and pediatricians. I have no hesitation in congratulating the contributors and commending the book in the highest terms.

Mohan Kameswaran MS FRCS FAMS DSc Adjunct Professor of Otolaryngology Tamil Nadu Dr MGR Medical University Chennai, Tamil Nadu, India Director Madras ENT Research Foundation Chennai, Tamil Nadu, India Member Executive Board, International Federation of Otolaryngological Societies Member Executive Board, Politzer Society Past President Asia Pacific Symposium on Cochlear Implants and Related Sciences Member Executive Council, National Academy of Medical Sciences, India Awarded Padma Shri by Hon’ble President of India

Foreword It gives me immense pleasure I am writing the foreword for Current Concepts of Otitis Media and Recent Management Strategies by Professor Anand Job. I have known Prof Anand Job for many years. He is an excellent teacher and dedicated academician and somebody I have looked up to in all my years as an ENT surgeon. This new book will be of use to postgraduates and practicing ENT surgeons alike. The highlight of the book is that each chapter sets out to explain the basic principles and seamlessly goes on to incorporate recent evidence pertaining to the topic. Some of the chapters require special mention. The chapters on “The Role of Eustachian Tube in Chronic Suppurative Otitis Media—Mucosal Disease”, and “Acute Otitis Media” and “Chronic Otitis Media” are especially written in great detail. Dedicated chapters covering etiopathogenesis and microbiology are well written and informative. Tympanoplasty and ossiculoplasty are organized in smaller, detailed chapters, covering a large number of practical points. With a lucid narrative, the author manages to get the fundamentals as well as relatively new concepts across in a easy and comprehensive manner. Meticulously illustrated pictures and ample photographs aid in better understanding of concepts, which students will find very useful. I would definitely recommend this book on Chronic Otitis Media—Mucosal Disease. The research and effort that have gone into the book are tangible in the form of an elegant, up to date textbook which I have no doubt will be a valuable addition in any ENT library.

Ravi Ramalingam Managing Director and Senior Consultant KKR ENT Hospital and Research Institute Chennai, Tamil Nadu, India

Foreword Otitis media continues to be a common problem in general practice especially in the pediatric population. It is therefore appropriate that another update of this disease is hitting the press. It’s a pleasure to compliment Dr Anand Job who, out of his wealth of experience, has written this book with a simple, elegant and eminently clinical approach. The book will be beneficial not only to the ENT fraternity but also to general practitioners, internists and mission hospital generalists as well. I wish the book every success. May its readership grow rapidly to enforce multiple editions of it, quickly.

Sunil Chandy Director Christian Medical College Vellore, Tamil Nadu, India

Preface It is our pleasure to present this book on Current Concepts of Otitis Media and Recent Management Strategies. The topics covered are from current literature as well as from personal experience. The emphasis has been to present the current diagnosis as well as medical and surgical management in a concise and comprehensive manner, useful for ENT practitioners in a developing country it can be used as learning material for ENT postgraduates as well as postgraduate teachers. Preventive aspects have been dealt with, focussing on pediatric patients with a view to reduce the burden of hearing loss as hearing disability can persist into adult life. The initial chapters deal with the pathogenesis of otitis media with special emphasis on the eustachian tube and its role in otitis media. Current definitions from various disease spectra of otitis media are presented along with relevant microbiology and pathology. Approach to children frequently affected is dealt from an immunological perspective also. Treatment options are discussed in their entirety with contraindications. Surgical management is discussed with specific emphasis on ossicular reconstruction using various types of titanium prosthesis. The reporting of outcomes of reconstruction has been simplified with view of an easy reporting system from surgical point of view. Rehabilitation of hearing loss with currently available devices has also been dealt with. Despite the fact that there are well established books on otitis media, the book hopes to bring together some of the newer developments in the management of the commonly seen disease in India. The objective has been to highlight some of the recent management strategies as well as recent advances, hoping to give readers relevant update and a better understanding of the disease process, because managing some of the resistant chronic ear diseases, can be quite challenging.

Anand Job L Paul Emerson

Acknowledgments This book was conceptualized and written by the inspiration given by my late father, Dr CK Job, who was an eminent scientist in the field of leprosy. We gratefully acknowledge our institution which encourages academic excellence and team work which promotes a positive atmosphere for patient care. Dr L Paul Emerson who has co-authored this book with me has been an inspiration and his contribution is of immense value. The book has been made possible by support from my colleagues Dr Rajiv Michael, Dr Regi Thomas, Dr Rajan Sundaresan, Dr Ajay Philip and Dr VK Anand for which we remain grateful as they have helped out in patient care during times when we were not available. We thank Dr Regi Thomas for his input in the initial stages of the book, Dr Rajan Sundaresan for the illustrations and Mrs Rama Prabha for secretarial help. We are also grateful to our colleagues, Dr John Mathew in ENT, Dr Winsely Rose in Child Health and Dr Shalini Anandan in clinical microbiology for their valuable input towards certain chapters in the book. We wish to acknowledge (Late) Dr Desmond who established the department and Dr Bhanu and Dr Raman (former HODs of ENT) who were our teachers. We thank Mr Tranter, ENT surgeon, United Kingdom for taking special efforts in my training in otology. We are also grateful to our friends, Dr Solomon Chelliah and Dr Samuel Chittaranjan for their support. We thank Mr Newton, Head, Dodd Memorial Library and Mr Jayanandan, Jaypee Brothers Medical Publishers, Chennai for their support. We are also indebted to our patients who travel long distances and go through many inconveniences in accessing our services and having faith in us. Most of all, we thank the Lord for his guidance.

Contents 1. History of Otitis Media

1

L Paul Emerson, Anand Job

2. Anatomy and Physiology of the Middle Ear

3

L Paul Emerson, Anand Job • • •

Endoscopic Anatomy of the Middle Ear Spaces 4 Sound Transmission 8 Ossicular Coupling  9

3. Eustachian Tube and its Role in Otitis Media

10

Anand Job, L Paul Emerson • • • • • • • •

Role of the Eustachian Tube in Chronic Otitis Media, Mucosal Disease 10 Evolution Effects on Immune System and on Eustachian Tube Function 10 Anatomy and Prenatal Growtht 10 Histopathology of Mucous Membrane of Tubal Lumen 11 Physiology of the Eustachian Tube 13 Tests of Eustachian Tube Function 18 Treatment 23 Management 25

4. Acute Otitis Media

29

L Paul Emerson, Anand Job • •

Clinical Diagnosis 30 Contribution of Acute Otitis Media to Chronic Otitis Media 32

5. Chronic Otitis Media Associated with Effusion

36

L Paul Emerson, Anand Job, John Mathew •

Classification of Post-Tympanostomy Tube Otorrhea 39

6. Chronic Otitis Media

43

L Paul Emerson, Anand Job

7. Chronic Otitis Media-Mucosal Disease Anand Job, L Paul Emerson • • • •

Etiopathology 47 Bacteriology 47 Investigations 48 Medical Treatment 48

47

20  Current Concepts of Otitis Media and Recent Management Strategies 8. Microbiology of Acute Otitis Media

51

Shalini Anandan, L Paul Emerson, Anand Job

9. Microbiology of Chronic Otitis Media

53

Shalini Anandan, Anand Job, L Paul Emerson

10. Pathophysiology of Chronic Otitis Media

55

Anand Job, L Paul Emerson •

Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and their Sequelae 56

11. Prevention of Acute Otitis Media

59

L Paul Emerson, Anand Job • • • • • • •

Approach to the Child with Recurrent Infections 59 Predisposing Factors 60 “Normal” Child 60 Child with Atopic Disease 61 Child with Chroknic Disease 62 Child with an Immunodeficiency 62 Management of Allergy 65

12. Vaccination for Preventing Acute Otitis Media

69

L Paul Emerson, Anand Job • •

Prevention of Recurrent Acute Otitis Media 69 Vaccine Schedule 70

13. Eosinophilic Otitis Media

72

L Paul Emerson, Anand Job •

Clinical Features 72

14. Preoperative and Intraoperative Considerations

76

Anand Job, L Paul Emerson, John Mathew •

Factors that Affect Surgical Decisions 76

15. Classification of Tympanoplasty

81

Anand Job, L Paul Emerson, John Mathew •

Classification of Tympanoplasty 82

16. Local Anesthesia for Middle Ear Surgery

84

L Paul Emerson, Anand Job • • •

Premedication 84 Adverse Effects of Lidocaine 86 Adverse Effects of Bupivacaine 87

17. Approaches for Tympanoplasty L Paul Emerson, Anand Job, John Mathew • • •

Transcanal Approach for Myringoplasty 88 Endaural Approach 88 Retroauricular Approach 88

88

Contents 21 18. Surgery of Tympanoplasty

103

Anand Job, L Paul Emerson, John Mathew • • • •

Myringoplasty 103 Type I Tympanoplasty 103 Type II Tympanoplasty 104 Type III Tympanoplasty 107

19. Tympanic Membrane Reconstruction Using Cartilage

110

Anand Job, L Paul Emerson, John Mathew • • • •

Classification of Cartilage Tympanoplasty 110 Class I 110 Class-II 113 Class-III 114

20. Ossicular Reconstruction

117

John Mathew, Anand Job, L Paul Emerson • • •

Porp and Torp in Ossiculoplasty 117 General Principles of Reconstruction 120 Total Ossicular Replacement Prosthesis 126

21. Hearing Aids

131

Swapna Sabastian, L Paul Emerson • • • • • • • •

Indications 131 Types of Hearing Aids 131 Digital Hearing Aid 134 Bone Conduction Retain Hearing Aid 134 Implantable Hearing Aid 136 Bone Conduction Implantable Hearing Aids 137 Bilateral Amplification 138 Cochlear Implant 138

Index 141

1

History of Otitis Media L Paul Emerson, Anand Job

INTRODUCTION The first published account to close the tympanic membrane (TM) perforation was in 1640, by Marcus Banzer1 who inserted a small ivory tube covered with pig’s bladder as a lateral graft. In 1841, Yearsley2 applied a ball of cotton wool moistened with glycerin against a TM perforation. In 1853, Toynbee3 placed a rubber disk attached to a silver wire over the TM and reported significant hearing improvement. In 1876, Roosa4 treated TM perforations with chemical cautery using silver nitrate to promote healing of the perforation which is the current practice for small perforations. In 1895, Okuneff started using trichloroacetic acid as the cauterizing agent, which is also used today. In 1877, Blake5 covered perforations with paper patches and this method is used for demonstrating the improvement in hearing likely to be achieved by tympanoplasty. The term ‘myringoplastiek’ was first coined by Berthold in 18786 and he used a full-thickness free skin graft for TM closure. Joynt7 combined cautery and paper patch techniques, which resulted in improvement in results of TM closure and was popularized by Derlacki.8 Since the introduction of tympanoplasty in the 1950s by Zellner and Wullstein, numerous graft materials have been used for the closure of the defective membrane such as skin, fascia lata, temporalis fascia, vein, perichondrium and dura mater. To date, temporalis fascia remains the most commonly employed material.9-11 In 1953, the Zeiss operating microscope became available commercially and in the same year, Wullstein and Zöllner, launched their tympanoplasty methods with a split-thickness skin graft at the Fifth International Congress of Otorhinolaryngology in Amsterdam. Later, Zollner described his experiences with a similar graft. In 1956, Zöllner successfully used autologous fascia lata. Heermann (1960)12 reported successful myringoplasty results using autologous temporalis fascia ‘onlay’ grafts and successful results were also reported using tragal perichondrium (Goodhill, Harris and Brockman, 1964) and using free autologous fat grafts (Ringenberg, 1962). Shea (1960)13 accidentally tore the TM during a stapedectomy procedure and repaired the tear successfully with a free autologous vein graft placed medial to the TM, thus introducing the ‘underlay’ technique of myringoplasty. In the 1960s and 1970s, homograft (cadaveric) materials, including TM, dura, and pericardium were used.

2  Current Concepts of Otitis Media and Recent Management Strategies Cartilage was first used in ossiculoplasty by Utechin (1959), as an interposition graft between the eardrum and the stapes, and in 1961, as a columella between the footplate and the eardrum. The first cartilage myringoplasty, using autologous septal cartilage, was performed by Salen in 1963. Jansen performed at the same time, myringoplasty with homologous septal cartilage plates without perichondrium. Currently, temporalis fascia continues to be used widely for repair of the TM although many surgeons are using conchal and tragal cartilage. For ossiculoplasty, titanium prosthesis is gaining wider acceptance over homologous ossicle or bone or cartilage.

REFERENCES 1. Banzer M. Disputatio de auditione laesa ‘Disertation on deafness’, 1640. 2. Yearsley J. Deafness practically illustrated, London: J Churchill and Sons, 1863. 3. Toynbee J. On the use of an artificial membrana tympani in cases of deafness dependent upon perforations or destruction of the natural organ. London: J Churchill and Sons; 1853. 4. Roosa DB. Diseases of the ear. New York: William Wood & Co.; 1876. 5. Blake CJ. Transactions of the first congress of the international otological society. New York: D. Appleton & Company; 1887.p.125. 6. Berthold E. About myringoplasty. Wien Med Blätter. 1878;26:627-39. 7. Joynt JA. Repair of drum. Iowa Med Soc. 1919;9:51. 8. Derlacki EL. Repair of central perforations of tympanic membrane. AMA Arch Otolaryngol. 1953;58(4):405-20. 9. Wullstein H. Theory and practice of tympanoplasty. Laryngoscope. 1956;66(8): 1076-93. 10. Wullstein HL. Functional operations in the middle ear with split-thickness skin graft. Arch Otorhinolaryngol. 1952;161:422-35. 11. Wullstein H. Surgery for hearing improvement, Uffenorde W. Anzeige und Ausführung der Eingriffe an Ohr, Nase und Hals. edn., Stuttgart: Thieme medical publishers; 1952.pp.227-58. 12. Herrmann H. Tympanic membrane plastic with temporal fascia. Hals Nas Ohrenh. 1960;9:136-40. 13. Shea JJ Jr. Vein graft closure of eardrum perforations. J Laryngol Otol. 1960;74: 358-62.

2

Anatomy and Physiology of the Middle Ear L Paul Emerson, Anand Job

INTRODUCTION The middle ear (ME)-conducting apparatus for hearing consists of the tympanic membrane (TM) and the three ossicles (Fig. 1).

Tympanic Membrane The orientation of the TM is slightly oblique to the sagittal plane. It is roughly conical in shape and pointing medially. The handle of malleus is attached to the medial aspect of the TM. The TM is divided into the pars flaccida, which is superior to the insertion of the manubrium and inferiorly, the pars tensa. The inferior end of the manubrium is called the umbo.

Malleus The manubrium or handle of malleus is attached to the pars tensa. It has an anterior process and lateral process. The head, which articulates with the incus, is in the epitympanic recess. The constriction between the manubrium and the head is called the neck of the malleus. The chorda tympani cross the medial surface of the malleus neck.

Fig. 1  Picture of the tympanic membrane

4  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 2  Middle ear ossicles

Incus The incus has a body and two processes, short and long. The body of the incus articulates with the head of the malleus in the epitympanic recess. At the end of the long process of the incus is a small region, the lenticular process, which articulates with the head of the stapes. The short process is attached to the cavity wall by the posterior incudal ligament.

Stapes The stapes has a footplate, two crurae, posterior and anterior, and a head. The head of the stapes articulates with the lenticular process of the incus. The footplate covers the oval window (Fig. 2).

ENDOSCOPIC ANATOMY OF THE MIDDLE EAR SPACES The recent developments in the field of otology include the study of the ME anatomical structures with Hopkins rod lens system or commonly called the endoscope. This has given a better understanding of the ME anatomy and its intricate structures and also the spread of pathology and its treatment. Initially they were used to visualize the nook and corners of the ME, which were difficult to see with a microscope especially in cholesteatoma clearance. But recent studies have suggested the use of endoscopes in common surgeries and understanding ME spaces gives great confidence to the otologic surgeon (Fig. 3). Middle ear and subspaces are generally divided into mesotympanum, i.e. medial to the TM, i.e. epitympanum; medial to the scutum and above

Anatomy and Physiology of the Middle Ear 5

Fig. 3  Use of endoscope for anatomy of middle ear: ST—sinus tympani

Fig. 4  Middle ear showing subspaces

mesotympanum; and hypotympanum below the mesotympanum; protympanum, i.e. anterior to the mesotympanum; and retrotympanum is that part of the ME that is posterior to the mesotympanum (Fig. 4). The divisions of mesotympanum are as follows: • Superior—epitympanum • Anterior—protympanum • Inferior—hypotympanum • Posterior—retrotympanum.

Retrotympanum The retrotympanum is the posterior part of the ME cavity. It contains a number of important structures that can be difficult to visualize during microscopic ear surgery (Fig. 5).

6  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 5 Various parts of retrotympanum: pe—pyramidal eminence; fn—facial nerve; jb—jugular bulb; p—ponticulum; pr—promontory; rw—round window; su—subiculum; ap—anteriorpillar; cp—cochleariform process; et—Eustachian tube; f—finiculus; pp—posterior pillar

The retrotympanum is divided into superior and inferior by the subiculum a bony ridge in the medial wall of the ME extending to the posteriorly. The different spaces are as follows:

Superior The space superior to subiculum has four spaces in relation to the vertical portion of facial nerve: • Two medially, in the anterior aspect, sinus tympani (ST) and posterior tympanic sinus • Two laterally, in the posterior aspect, facial sinus and lateral tympanic sinus.

Inferior The space inferior to the subiculum is the sinus sub tympanicus that has been less understood and is now well-established by endoscopic visualization (Fig. 6).

Subpyramidal Space Subpyramidal space is a space under the pyramidal process and is also prone for persistence of cholesteatoma. There are variations in this space, which leads to residual disease (Fig. 7). One of the most important structures in retrotympanum is the ST. This cavity is sinus tympani between the medial walls of the ME medially and the pyramidal

Anatomy and Physiology of the Middle Ear 7

Fig. 6  Showing different spaces present in the retrotympanum: pe—pyramidal eminence; fn—facial nerve; p—ponticulum; pr—promontory; ps—posterior sinus; rw—round window; su—subiculum; st—sinus tympani

Fig. 7  Endoscopic anatomy of retrotympanum: pe—pyramidal eminence; fn—facial nerve; ps—posterior sinus; st—sinus tympani

eminence (PE) laterally, with the VII nerve posterolaterally. It is bound superiorly by the ponticulus and inferiorly by the subiculum. When cholesteatoma involves the retrotympanum, especially the ST, there may be two important issues: 1. The potential for residual disease due to incomplete removal of disease for lack of adequate exposure. 2. The risk of ossicular dislocation and hearing loss caused during removal of cholesteatoma within a space not easily visualized by microscopic techniques.

8  Current Concepts of Otitis Media and Recent Management Strategies Recently, endoscopes have made possible fresh understanding of the ME, especially the retrotympanum.

Facial Nerve Facial nerve is an important structure that traverses the ME posterior to the retrotympanum. Housed in a bony canal the nerve passes in a horizontal plane, as it enters the ME and turns inferiorly at the posterior end of the mesotympanum and travels in a vertical plane. It is important to understand the various inner ear structures in relation to the facial nerve.

SOUND TRANSMISSION The acoustic resistance to the passage of sound through a medium is termed impedance. The transduction of vibratory energy from the air in the external auditory canal (low impedance) to the cochlear fluids (high impedance) is possible as a result of the impedance-matching function of the ME. The TM and the three levers accomplish the required pressure transformation for transduction. 1. Catenary lever: The impedance matching mechanism, the catenary lever action, curved membrane effect or buckling effect of the TM, was first explained by Helmholtz (1868), who observed that the umbo of the TM is displaced less than the remaining surface of the TM. Since, the outside edge of the membrane is firmly attached to the annulus and curves medially to attach to the umbo, the displacement of the membrane between the annulus and umbo is larger than at the umbo (Tonndorf and Khanna, 1970). This creates a lever action, which increases the force acting at the umbo by approximately two times or 6 dB (Rosowski, 1996). The principle of this mechanism is shown in Figures 8A and B. 2. Ossicular lever: The malleus and incus acting as a unit rotate around an axis running between the anterior mallear ligament and the incudal ligament. The gain of the ossicular lever is the length of the manubrium of the malleus divided by the length of the long process of the incus (approximately 1.3:1). The ossicular lever taken alone produces a small mechanical advantage for sound transmission. The catenary lever is tightly coupled to the ossicular lever, because the TM is extensively adherent to the malleus handle.

A

B

Figs 8A and B  (A) Ossicular level mechanism (Hydraulic lever); (B) Cantenary lever mechanism

Anatomy and Physiology of the Middle Ear 9 Corrected calculations arrive at a combined catenary-ossicular lever ratio of 1:2.3. 3. Hydraulic lever: The hydraulic lever acts because of the size difference between the TM and the stapes footplate. Sound pressure collected over the area of the TM and transmitted to the area of the smaller footplate results in an increase in force proportional to the ratio of the areas. The average ratio has been calculated to be 20.8:1. Taking the three levers together, the ME offers a theoretical gain of approximately 34 dB.

OSSICULAR COUPLING Ossicular coupling refers to the true sound pressure gain, which occurs through the actions of the TM and the ossicular chain. The true gain of the ME is less than the theorized 34 dB. The pressure gains provided by the normal ME with ossicular coupling is frequency dependent. The actual mean ME gain is 20 dB at 250–500 hertz (Hz), reaching a maximum of 25 dB at 1 kilohertz (kHz), and then decreasing at about 6 dB per octave at frequencies above 1 kHz. The changes in gain above 1 kHz are caused by portions of the TM moving differently than other portions, depending on the frequency of vibration. At low frequencies, the entire TM moves in one phase. Above 1 kHz, the TM divides into smaller vibrating portions that vibrate at different phases. Another factor is slippage of the ossicular chain, especially at frequencies above 1–2 kHz. Slippage is due to the translational movement in the rotational axis of the ossicles or flexion in the ossicular joints. Some energy is lost in sound transmission, because of the forces needed to overcome the stiffness and mass of the TM and ossicular chain.

BIBLIOGRAPHY 1. JoãoFlávioNogueira, Francesco Mattioli, LivioPresutti, Daniele Marchioni. Endoscopic anatomy of the retrotympanum review article otolaryngologic clinics of North America. 2013;46(2):179-88. 2. John J. Rosowski, Albrecht Eiber AudiolNeurootol. 1999;4:121–22, Accessible online at: http://BioMedNet.com/karger 3. Shambaugh,Text book of Ear Surgery. McGraw-Hill Medical; 6 edition. 4. Tonndorf J, Khanna SM. The role of the tympanic membrane in middle ear transmission. Ann Otol Rhinol Laryngol. 1970;79(4):743-53.

3

Eustachian Tube and its Role in Otitis Media Anand Job, L Paul Emerson

ROLE OF THE EUSTACHIAN TUBE IN CHRONIC OTITIS MEDIA, MUCOSAL DISEASE The eustachian tube (ET) being located at the skull base, has been an inaccessible organ for studies and therapy until recently, by means of imaging, diagnostic endoscopy and endoscopic surgery. The ET connects the nasopharynx with the tympanic cavity and is likened to an organ consisting of a lumen with its mucosa, cartilage, surrounding soft tissue, paratubal muscles [i.e. tensor veli palatini (TVP), tensor tympani, levator veli palatini (LVP) and salpingopharyngeus] and bony support.

EVOLUTION EFFECTS ON IMMUNE SYSTEM AND ON EUSTACHIAN TUBE FUNCTION Humans appear to be the only species that develops otitis media. It is wellknown that we are born early, which is the result of adaptations to bipedalism and our larger brain and a relatively small female pelvic outlet compared with nonhuman primate.1 As a consequence of too early birth, our immune system is relatively immature and also the ET is too short and floppy during the first year of life, which predisposes us to middle ear infections. The other adaptation was the descent of the larynx, which along with a decrease in prognathism (i.e. facial flattening), resulted in a change in palatal morphology as compared with other primates. Also, primate have superior function of the levator veli palatini muscle (LVPM).2

ANATOMY AND PRENATAL GROWTH As the fetal cranial base is relatively flat, the tube deviates from the horizontal plane only about 10°, a condition that persists into early childhood, which has clinical implications. During postnatal development, the cranial base angle and the vertical dimensions of the skull increase. The hard palate drops away from the skull base. As this occurs, the angle between the cartilaginous tube and the skull base increases to reach an angle of 45° (Table 1, Fig. 1). The difference in the angle of the ET in the infant and adult affects the function of the tensor veli palatini muscle (TVPM), which is the principal dilator of the ET. The ET can be divided into three portions: 1. Cartilaginous. 2. Junctional. 3. Osseous.

Eustachian Tube and its Role in Otitis Media 11 Table 1  Differences in eustachian tube—children—adults Cartilage cell density

Greater

Less

Elastin at hinge portion of cartilage

Less dense—affects closure

More—better closure

Ostmann’s fat pad

Less

Large

Mucosal folds

Greater

Lumen glands

Variable type

Middle ear volume

Smaller

Lumen

Small

Cartilage volume

Less

More

Source: The eustachian tube: Structure function and role in the middle ear; Charles D Bluestone.

Fig. 1 The eustachian tube-middle ear system in which the pharynx, palate and nasal cavities are proximal to the tube and, at the distal end of the system, the middle ear and mastoid gas cells (Source: Bluestone CD. Conquering otitis media. Hamilton (ON): BC Decker; 1999)

The cartilaginous portion is proximal and opens into the nasopharynx. The osseous portion is distal and opens into the anterior middle ear. The junctional portion is that part of the tube where the cartilaginous and osseous portions connect. A three-dimensional (3D) study of nine human temporal bone specimens by Sudo and colleagues,3 have demonstrated that the isthmus portion of the lumen to be near the distal end of the cartilaginous portion and not at the junction of the cartilaginous and osseous portions.

HISTOPATHOLOGY OF MUCOUS MEMBRANE OF TUBAL LUMEN (FIG. 2) The tubal lumen is lined by pseudostratified ciliated columnar epithelium, which sweeps material from the middle ear to the nasopharynx. The mucosa is

12  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 2  Artistic representation of representative cells in the mucous membrane of the middle ear and eustachian tube (Source: Lim DJ. Functional morphology of the mucosa of the middle ear and eustachian tube. Ann Otol Rhinol Laryngol.1976;85:36-43)

continuous with the lining of the tympanic cavity at its distal end and with the nasopharynx at the proximal end. Goblet cells are associated with these ciliated epithelial cells and compose about 20% of the cell population.4

Goblet Cells Tos and Bak-Pedersen,5 studied temporal bones from premature and newborn infants, children and adults who were free of signs of otitis media and found counts from 30,000 up to 60,000 goblet cells in different portions of the ET. Low densities were found in all parts of the tube in premature infants with gradually increasing densities in the pharyngeal portions through childhood and high densities in adults. Higher densities were reported in the lateral and medial walls and in the floor of the tube, but lower densities were found in the roof. Sando and colleagues described more mucosal folds in the inferior half than in the superior half of the ET as well as more numerous ciliated cells, glands and goblet cells. From these findings, they postulated that the superior portion of the

Eustachian Tube and its Role in Otitis Media 13 lumen is probably involved in ventilation (i.e. pressure regulation) and the lower portion is related to the clearance function of the tube.

Mucosa-associated Lymphoid Tissue and its Role in Eustachian Tube Obstruction Mucosa-associated lymphoid tissue (MALT) is scattered along mucosal linings in the human body6–8 and constitutes the most extensive component of human lymphoid tissue. These surfaces protect the body from an enormous quantity and variety of antigens. The tonsils and the Peyer’s patches within the small intestine are examples of MALT. The ET mucosa originates from the same ectoderm as upper respiratory tract mucosa. The lymphoid follicles in the ET develop by extravasations’ of lymphocytes from the postcapillary high endothelial venule, into the mucosal inflammatory sites. Mucosa-associated lymphoid tissue is found submucosally throughout the ET and is prominent around the inferior half of cartilaginous tube, which may be an important factor for obstruction of the lumen during infections. Kamimura9 and colleagues found that MALT has a close relationship to otitis media and might be a local response to recurrent infection in the ET and middle ear. Aginomori10 and colleagues hypothesized that cellular proliferation of MALT within the middle ear and ET might reflect the activity that produces immunoglobulin A against invasion of foreign antigens. The MALT was found more abundantly in the osseous portion of the ET and middle ear when middle ear infection had been present. Ozturk et al11 who had studied cadaver specimens of the ET of children and adults, found that the posterior wall of the ET had more mucosal folds (described as microturbinates) than the anterior wall. These microturbinates may lead to air turbulence and contribute to the clearance and protection functions of the ET by trapping of particles such as microorganisms and foreign bodies like nasal turbinates. After completion of growth and ET development, the microturbinates become smaller and atrophic. In conclusion, it is suggested that the superior part of the ET is mainly involved in ventilation, whereas the lower part is mainly involved in clearance and protection function.

PHYSIOLOGY OF THE EUSTACHIAN TUBE (FIG. 3) Normal middle ear pressure is vital for maintaining the anatomical and functional qualities of the middle ear conductive mechanism, especially the tympanic membrane. The middle ear mucosa ensures permanent gas exchanges with a tendency towards gas loss from the middle ear cavity into the blood. These gas exchanges normally lead to a constant decline in the pressure in the middle ear cavity. The main function of the ET is to restore balance of this pressure and also to aid in mucociliary clearance from the middle ear.

Protective Function (Fig. 4) The ET is usually closed at rest. Sudden loud sounds are, therefore, dampened before reaching the middle ear through the nasopharynx. Also, secretions from

14  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 3  Physiology of the eustachian tube

Fig. 4  The protective function of the eustachian tube is primarily due to its anatomy in that narrow portion, and the physiologic middle-ear gas (air) cushion prevents nasopharyngeal secretions from entering the middle ear

the nasopharynx cannot reflux into the middle ear easily. The middle ear is also protected by the local immunologic defense of the respiratory epithelium of the ET. A pulmonary immunoreactive surfactant protein has been isolated from the middle ears of animals and humans and is thought to have some protective function in the middle ear.12

Eustachian Tube and its Role in Otitis Media 15

Clearance Function Drainage of secretions and occasional foreign material from the middle ear is achieved by the mucociliary system of the ET and the middle ear mucosa, muscular clearance of the pharyngeal portion of the ET and the surface tension within the tubal lumen.

Flask Model (Fig. 5) Flask model was proposed by Bluestone and his colleagues,13 and helps to better explain the role of anatomic configuration of the ET in protection and drainage of the middle ear. In this model, the ET and middle ear system is likened to a flask with a long narrow neck. The mouth of the flask represents the nasopharyngeal end; the narrow neck represents the isthmus; and the middle ear and mastoid air cell system represents the body of the flask. Flow of fluid through the neck depends on the pressure at end, the radius and the length of the neck and viscosity of the liquid. In children, the ET has a much shorter neck. As a result, less pressure is required at the nasopharynx to force fluid and pathogens into the middle ear. In an erect adult, the ET inclines about 45° to the horizontal plane, whereas in a child, it is only about 10°. Thus, in an adult, the benefit of gravity acts to increase resistance to fluid entering the middle ear. Conversely, an infant/child gains little benefit, because the tube is nearly perpendicular to the force of gravity. Moreover, an infant feeding in the supine position actually has the full force of gravity driving fluid into the middle ear.

Fig. 5  The flask model of the middle-ear system for fluid flow through a flask with a compliant neck. (A) Fluid stopped in the neck of the flask; (B) Effect of negative pressure applied slowly to the bottom of the flask; (C) Effect of negative pressure applied suddenly to the bottom of the flask (Source: Bluestone CD. Conquering otitis media. Hamilton (ON): BC Decker; 1999)

16  Current Concepts of Otitis Media and Recent Management Strategies

Pressure Regulation Function by Tubal-opening Mechanism (Fig. 6) The two tubal muscles are: 1. Levator veli palatini muscle. 2. Tensor veli palatini muscle. These are the main tubal dilators, which ensure ET function. The LVPM constitutes the floor of the ET and causes rotation of the tubal cartilage and the proximal opening of the tube. According to Isshika et al even though the LVPM lies close to the medial lamina (ML), it does not have any attachment; however, due to the superior medial rotation of the ML, it causes the opening of the cartilaginous portion (anterior) of the ET. They also state that, since the contraction time of LVPM is longer than TVPM, the anterior cartilaginous portion may remain open longer even after the closure of posterior and middle portions, which are closed due to relaxation of TVPM, thus producing a protective pumping-like mechanism from middle ear to nasopharynx, which prevents nasopharyngeal secretions from entering the middle ear. The tensor tympani muscle also plays a specific role in the tubal-opening mechanism.14 The tensor tympani is attached to the neck of the malleus and contraction of the muscle may slightly increase the middle ear pressure by medial displacement of the tympanic membrane. The origin of this muscle is from the cartilage of the tube and the adjoining bone and can influence the opening of the tube at the isthmus (Ingelstedt and Jonson, 1966).15 Thus, contractions of the tensor tympani may play an important role in the tubal-opening mechanism, especially at the isthmus.

Fig. 6  Pressure regulation function: during swallowing, the normal eustachian tube opens (dilates) by contraction of the tensor veli palatini muscle, equilibrates pressure between the nasopharynx and the middle ear and mastoid gas cells (Bluestone CD. Conquering otitis media. Hamilton (ON): BC Decker; 1999)

Eustachian Tube and its Role in Otitis Media 17 Another mechanism for opening the ET is the middle ear pressure. If the intratympanic air pressure for some reason exceeds 100–150 mm H2O above the ambient air pressure, the ET can open spontaneously without any muscular activity. Also, when increased pressure is applied from the nasopharyngeal end, the ET opens. This is exemplified in tubal catheterizing or in applying high pressure in the nasopharynx as in the Valsalva maneuver.

Tubal Opening Time The equalization capacity of the tube is influenced by many factors among which the most critical seems to be, the time the tube stays open as a result of muscular activity or air pressure influence. According to many investigators (Perlman, 1951; Miller, 196517; Flisberg, 196616), the opening time varies between 0.1 sec and 0.9 sec. Depending on the pressure difference across the tube, the width and length of the narrowest part, together with the opening time, the air volumes passing through the tube may vary. This explains the great differences in tubal ventilating functions, even among normal persons.

Tubal Closing Mechanism In contrast to opening of the tube, closure is exclusively a passive phenomenon. When the muscles relax or when a static pressure no longer keeps, the tubal walls separated and the tubal lumen collapses. Closure proceeds from distal to proximal, i.e. from the valve area to the nasopharyngeal end. This mechanism is hypothesized to have a protective effect against reflux.29

Eustachian Tube Function at Changing Ambient Pressure The response of the ET to changes in the ambient pressure has been studied by many authors (Thomsen, 195817; Ingelstedt et al 196718). When ambient air pressure decreases, as during flight ascent, the intratympanic air pressure increases. Opening of the ET is now facilitated on swallowing or the tube may even open spontaneously as a response of the air pressure force on the tubal walls. The situation is more complex when the relative intratympanic air pressure is decreasing, as during descent. The increased negative middle ear pressure up to at least 150 mm H2O facilitates tubal opening (Filsberg, 1966). It has also been shown that a negative middle ear pressure of about 1,100 mm H2O may make it impossible for the tubal opening muscles to overcome the collapsing force and locking the tube. These observations are especially relevant for divers and pilots exposed to rapid and great changes of the ambient air pressure and also important to those with chronic ear disease with eustachian tube dysfunction (ETD).

Eustachian Tube Dysfunction (ETD) in Relation to Middle Ear Inflammation (Fig. 7) Eustachian tube dysfunction occurs when the tube fails to open properly or becomes blocked, thereby preventing the normal flow of air into the middle ear. The acts of swallowing or yawning are usually enough to momentarily open the

18  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 7  Loss of the protective function of the eustachian tube can occur if the tubal lumen is too open. Nasopharyngeal secretions can reflux into the middle ear (Bluestone CD. Conquering otitis media. Hamilton (ON): BC Decker; 1999)

ET, allowing it to regulate air pressure. However, it is possible that these actions are no longer sufficient, either because the ET is blocked or because it cannot respond to a greater demand from the middle ear when gas exchanges become more marked, such as during the average ear inflammation. This is known as ETD. Anatomic abnormalities such as cleft palate and other craniofacial abnormalities lead to inflammation of the ET causing ETD. Anatomical obstruction of the pharyngeal portion of the ET, due to enlarged adenoids or mass in the nasopharynx, congenital or acquired stenosis of the ET, can also cause ETD. The ET pathology is strongly related to mucosal disease and associated hypertrophy, which can be precipitated by reactive disease (e.g. allergy). Damage to the tubal lining also can be directly related to viral infection, which is thought to result in decreased mucociliary clearance. Viral infection can precipitate a bacterial inflammation of the middle ear cleft, with increased oxygen demands and an inflamed ET leading to ETD. Immune deficiency and chronic adenoiditis cause recurrent infections of the ET. Gastroesophageal reflux19 and sinusitis also play a role in the development of middle ear and ET inflammation causing ETD.

TESTS OF EUSTACHIAN TUBE FUNCTION Valsalva Test In the Valsalva test, the ET and middle ear are inflated by a forced expiration with the mouth closed and the nose pinched by the thumb and forefinger. The effect of high positive nasopharyngeal pressure at the proximal end of the ET system can be evaluated qualitatively. When the tympanic membrane (TM) is intact, the overpressure in the middle ear can be observed by otoscopy as a bulging TM.

Eustachian Tube and its Role in Otitis Media 19 When the TM is perforated, the sound of the air escaping from the middle ear can be heard with a stethoscope or with the Toynbee tube.

Politzer Test The Politzer test is similar to the Valsalva test, but instead of positive nasopharyngeal pressure being generated by the patient, the nasopharynx is passively inflated. This is achieved by compressing one nostril into which the end of a rubber tube attached to an air bag has been inserted while compressing the opposite nostril by finger pressure. The subject is asked to swallow or to elevate the soft palate by repeating the letter ‘k’. Valsalva continues to be used as a quick outpatient test to assess ETD. The Politzer test is outdated and rarely used clinically for assessment of ET function.

Toynbee Test The Toynbee test is considered more reliable than the Valsalva and Politzer tests in the assessment of ET function. On closed nose swallowing, negative middle ear pressure develops in healthy persons. In an intact TM, pneumatic otoscopy or tympanometry can be used to measure changes in the middle ear compliance. In a perforated TM, the manometer of the impedance bridge can be used to measure middle ear pressure changes.

Tympanometry Measuring middle ear pressure with an electro-acoustic impedance meter helps to assess ET function. High negative middle ear pressure (>100 dPa) indicates ETD. Bluestone20 provided a nine-step inflation-deflation ET assessment procedure for intact TMs. This procedure involves swallowing maneuvers at both positive and negative pressures. One’s ability to cause at least a 20 mm pressure change, as measured on the tympanogram was the criterion for adequate tubal patency. This technique also has a modification for nonintact TMs. The procedure is based upon the application of positive pressure to the middle ear until the ET spontaneously opens. The manometer is then stopped and observed regarding the pressure at which the ET passively closes. The patient is then asked to swallow to equilibrate the remaining pressure. The procedure may also be used with negatively induced pressure by asking the patient to equilibrate the pressure with swallows. This technique has provided a vehicle for numerous researchers and clinicians in the study of ET patency.

Sonotubometry Sonotubometry measures the function of the ET using sound. A constant sound source is applied to the nostril, while a microphone in the external auditory canal records the transmitted sound pressure level. When water is swallowed, opening of the tube is reflected by a sudden increase in signal in the external ear canal (5 dB).

20  Current Concepts of Otitis Media and Recent Management Strategies However, as the results tend to be ambiguous in children and because otitis media is most common in this population, although there are great advantages over other function tests, it is not used routinely to assess ET function.

Imaging The ET may be radiologically viewed using lipiodol ultrafluid as a contrast medium.21,22 The dye is injected through an intact TM or through a perforation or tympanostomy tube. The X-rays are taken immediately and after 10 minutes of installation in Stenver’s frontal and submentovertex positions. The 3D computed tomography (CT) scans with multiplanar reconstruction have also been used to assess the tube in normal individuals, in patients with patulous (P) ET23 and in otitis media.24 Fluoroscopy with contrast studies provide dynamic evaluation of mucociliary clearance. Functional magnetic resonance imaging (MRI)25 is yet another innovation in the assessment of ET function. For anatomical evaluation of the auditory tube and its surrounding structures, a T2-weighted turbo spin-echo sequence (axial orientation, TR/TE 3194/100 ms; coronal orientation TR/TE 3993/100 ms, NEX:4) and a T1-weighted 3D gradient-echo sequence (TR/TE:42/4.6 ms, slice thickness 1 mm, axial orientation pre and postintravenous injection of contrast material) can be carried out. In order to assess the opening of the auditory tube a single slice dynamic turbo gradient-echo sequence (TR/TE 15/6.5 ms, flip angle 15°, SPIR pulse, matrix 256 × 256, FOV 240 mm, slice thickness 5 mm, NEX:2) is performed, while the patient performs a Valsalva maneuver.

Trans-ET Endoscopy Kimura et al were the first authors to introduce trans-ET endoscopy in 1989.26 In 1994, Edelstein et al27 passed a flexible, micro fiberoptic endoscope through the ET via its pharyngeal orifice for evaluating the middle ear status. As there was significant instrument failure from internal breakage of the fibers, the procedure was not acceptable. Linstrom et al26 performed trans-tympanic ET endoscopy on patients with chronic ear disease, using flexible fiberoptic endoscopes of 0.5 mm and 1.0 mm diameter and found the lumen at the isthmus substantially narrowed in those with chronic otitis media (COM).

Transnasal Endoscopic Evaluation of Eustachian Tube Poe et al28 evaluated ET function using a rigid nasal telescope having the advantage of a larger diameter endoscope, when placed in the nasopharynx at the correct angle allowed one to look superiorly and laterally up the ET orifice to observe it during active dilation. As the endoscope did not interfere with the ET motion, a dynamic study was possible. The 4 mm flexible fiberoptic endoscope also yielded a very good view capable of slow motion video analysis and was easier to position, to see the ET orifice than a rigid scope of comparable size. However, the best optics were provided by 4 mm rigid endoscopes, which yielded clear large images that were well-suited to examination of fine muscular movements in the lumen, as it opened during maneuvers.

Eustachian Tube and its Role in Otitis Media 21

Procedure In the sitting position, topical anesthetic with decongestant, lidocaine 4% with oxymetazoline, is sprayed into both nasal cavities, while the patient sniffs. The endoscope is introduced into the nasal cavity and advanced up to the nasopharyngeal orifice of the ET, just posterior to the inferior turbinate and the ET recognized by the torus tubarius. It is easy to pass by the torus and examine the fossa of Rosenmuller, mistaking it to be the ET orifice. Once at the orifice, the endoscope is rotated slightly to look superiorly toward the long axis of the tube. The optimal fiber-optic view is obtained by introducing the endoscope along the floor of the contralateral nasal cavity and passing the tip behind the vomer. This brings the tip into the proper angle to view up the long axis of the ET, when it dilates. Video recordings are made with the patient vocalizing ‘K-K-K’ repeatedly to isolate the action of the LVP from the TVP. The ‘Ks’ stimulate palatal elevation and posteromedial rotation of the medial cartilaginous lamina and posteromedial wall of the ET. Swallows are done to induce normal physiologic tubal dilations and forced yawns are performed to cause maximal sustained dilation. The video of tubal dilations is reviewed and analyzed in normal time, slow motion and even stepping through single frames that are captured at a rate of 30 frames/ second.

Normal Eustachian Tube-opening on Endoscopic Evaluation (Figs 8A to C) Normal dilation and opening were observed to have four consistent sequential phases during a normal swallow:29 1. The soft palate elevates with simultaneous medial rotation of the posteromedial wall of the ET. The lateral pharyngeal wall also medialises, causing transient constriction of the nasopharyngeal orifice despite the medial rotation of the ET medial wall. One hypothesis for this contrary movement could be to provide momentary protection of the ET against reflux at the initiation of swallow. 2. The palate remains elevated and the posteromedial wall remains medially rotated, as the lateral pharyngeal wall displaces laterally to begin the dilation of the nasopharyngeal orifice. 3. The TVP begins to contract, causing dilation of the lumen to propagate from the nasopharyngeal orifice toward the bony isthmus. The dilation occurs by displacement of the anterolateral tubal wall laterally and away from the already contracted and medially rotated posteromedial wall. 4. Tubal opening occurs as the functional valve of the cartilaginous tube dilates into a roughly rounded aperture. The convex bulge seen in the resting anterolateral valve wall becomes visibly flattened to produce the final opening. 5. Closure of the tube begins with closure of the valve area and propagates proximally toward the nasopharyngeal orifice. This distal to proximal closure has been hypothesized to have a pumping action that may protect against reflux.

22  Current Concepts of Otitis Media and Recent Management Strategies

A

B

C Figs 8A to C  (A) Right eustachian tube in relaxed state; (B) Location of the tensor veli palatini (TVPM) and levator veli palatini (LVPM) muscles before their contraction; (C) Opening of the eustachian tube secondary to the voluntary contraction of the TVPM and LVPM muscles

On video endoscopic assessment of the pharyngeal opening of the ET, Poe et al found that normal subjects showed significant variations in several static and dynamic properties of the ET. There was a wide range in the mucosal thickness, mucosal folds and patency of the pharyngeal orifice at rest, and thickness of the isthmus valve convexity, most likely due in part to Ostmann’s fat pad. Thin subjects had consistently thin mucosa and obese subjects had significant thick lumen walls. During active swallowing or yawning, there were large variations between patients in the degree of motion of the medial cartilaginous lamina, lateral excursion of the lateral pharyngeal wall and height of palatal elevation. The mucosal and muscular motion variations became minimal moving from proximal to distal and approaching the region of the isthmus. Recent studies of the peritubal musculature show that opening occurs principally by the coordinated action of the TVP and a group of adjacent muscle fibers called the dilator tubae muscle.30 The dilator tubae muscle originates primarily on the lateral membranous wall of the ET, intermingles with the more medial TVP fibers, courses adjacent to the TVP tendon and then loosely wraps around the middle third of the hamulus and inserts beyond the hamulus into the velum. The dilator tubae has no bony insertion and is completely dependent on TVP contraction as a platform against which the dilator can open the tube. The TVP, therefore, has significant control over the efficiency of tubal dilation.

Eustachian Tube and its Role in Otitis Media 23 The action of the LVP is to elevate the palate and medially rotate the medial cartilaginous lamina. These actions begin the distal dilation of the ET and set the stage for the subsequent TVP contraction. The TVP can be seen to contract by the ripple of tension that lateralizes the lateral membranous wall. Once the entire distal tube is open, the final act appears to be the dilator tubae muscle pulling the valve-like convexity of the lateral wall at the isthmus, laterally to open the full length of the tube. The bony portion is normally patent at all times. The lumen of the maximally dilated tube appeared nearly circular. The relaxation sequence began with closure of the isthmus convex valve and then closure of the tube from distal to proximal. Mathew GA et al31 in a study done on 61 normal ears and 63 ears with middle ear disease, classified patterns of ET function on video endoscopy are as follows: 1. Grade 0: Normal ET with no mucosal edema or congestion. Medial cartilaginous lamina and lateral wall movements are normal. Tubal lumen opens well on swallowing. 2. Grade 1: Edema and congestion of mucosa limited to the pharyngeal orifice of ET. Normal lateral wall motion and tubal lumen opens with swallowing. 3. Grade 2A: Reduced lateral wall motion secondary to edema and congestion involving lumen. Tubal lumen opens partly with swallowing. 4. Grade 2B: Reduced lateral wall motion secondary to abnormal tubal muscle contraction. Tubal lumen opens partly with swallowing. 5. Grade 3A: Tubal lumen fails to open with swallowing secondary to gross edema. 6. Grade 3B: Tubal lumen fails to open with swallowing secondary to abnormal tubal muscle contraction. Patulous (P): Noticeable concavity in the superior portion of the lateral wall of the lumen, with persistent patency of the lumen, extending towards the isthmus, with medial and lateral cartilaginous walls remaining separate even at rest. The study showed a significantly higher prevalence of ETD among individuals with middle ear disease compared to the control group and significant correlation between manometric studies (positive pressure equalization test and tympanometry) and ET video endoscopy.

TREATMENT The treatment of ETD is directed at the underlying etiology.6 The choice of management strategies for isolated ETD remains controversial as randomized trial data are limited, study outcomes variable and much of what is known about the treatment is from animal rather than human studies.32,33 In a systematic review of 34 observational studies and randomized trials assessing a variety of interventions (e.g. decongestants, antibiotics and surgery), several studies demonstrated beneficial effects for some aspects of tubal function (mostly ventilatory function) and detrimental effects for others (mostly protective and/or clearance functions). There was no intervention that was consistently effective in improving tubal function. Dilatory dysfunction should be differentiated from patulous dysfunction, as ear blockage symptom can occur in both. Dilatory dysfunction treatments for patulous dysfunction will fail to help and may even exacerbate the symptoms.

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Dilatory Dysfunction Underlying Etiologies The eustachian tube dilatory dysfunction is most commonly caused by inflammation related to the underlying etiology. In the absence of bacterial infection, systemic decongestants (most commonly pseudoephedrine and phenylephrine), antihistamines or nasal steroid sprays are frequently prescribed to treat presumptive viral rhinosinusitis or allergic rhinitis. 1. Rhinosinusitis: Treatment for viral rhinosinusitis and mild cases of bacterial rhinosinusitis is usually directed at symptom management. Moderate to severe cases of acute bacterial rhinosinusitis are usually treated with antibiotics. Additionally, multiple therapies are utilized in the management of chronic rhinosinusitis, including intranasal saline, topical and sometimes systemic glucocorticoids (to be used with caution), antibiotics, leukotriene inhibitors and antifungal medication. Allergies can be partly controlled by avoidance of the offending agents. Pharmacotherapy varies based on patient age, severity of symptoms and comorbidities (e.g. asthma, nasal polyposis). Antihistamines, topical nasal steroid sprays, oral leukotriene inhibitors or combinations of these treatments are commonly effective in treating allergic symptoms. Immunotherapy can be helpful in refractory cases. Counseling for smoking cessation and the hazards of secondhand smoking should also be offered to the patient. In children over 6 years old with otitis media with effusion (OME), allergies should be strongly suspected. Patients with vasomotor rhinitis may have allergies that have not been identified by testing and may respond to the above measures as well. 2. Laryngopharyngeal reflux: Treatment should begin with behavioral modification. This includes avoidance of caffeine, alcohol, chocolate, peppermints, carbonated beverages, nicotine and spicy foods. Patients should eat smaller meals and avoid eating immediately before exercise or sleep. Patients with concomitant laryngopharyngeal and gastroesophageal reflux disease (GERD), should be treated with proton pump inhibitors. For all other patients, in the absence of symptomatic GERD, acid-blocking therapy is generally not helpful. 3. Obstructive-mass lesions: Mass lesions blocking the ET are treated according to the nature of the mass. Adenoid hypertrophy is the most common cause in children, which the adenoid either physically impairs the opening of the tubal orifice or it may contribute to inflammation within the ET. Excision of enlarged adenoids is effective in reducing the incidence of OME, especially in children. Tumors are common, but should be suspected in cases of persistent unilateral symptoms. Nasopharyngeal carcinoma, the most common malignancy affecting the ET, is treated in consultation of the radiation oncologists. 4. For decongestion of ET, oxymetazoline and xylometazoline were found to be beneficial in middle ear.34 There is little evidence to support the use of pharmacologic therapies for isolated ETD. Systemic decongestants such as pseudoephedrine or phenylephrine may be helpful for congestive symptoms (e.g. ear fullness or pressure), particularly in patients with a retracted tympanic membrane.

Eustachian Tube and its Role in Otitis Media 25 Systemic or topical decongestants are not effective in cases of OME. Topical nasal decongestant sprays or drops may be used on a limited basis (generally 3 days or less) for symptomatic relief of nasal congestion or rhinitis, with or without ear blockage symptoms. Topical decongestants may also be helpful for difficulty in clearing the ears during flights and scuba diving. Patients should be counseled within 3 days of nasal decongestant treatment, in order to avoid nasal mucosal dependency and rhinitis medicamentosa. A Cochrane review of OME for use in children identified 16 randomized controlled trails (RCTs) that included over 1,800 subjects.19 The effects on multiple short- and long-term outcomes repeatedly demonstrated no benefit for use of these medications over placebo for treating OME. Additionally, the reviewed studies found evidence of increased side effects and harms with the use of these medications. Topical steroid drops are being used in Europe, but the efficacy has not been established. Inhalation of steam is often suggested, but has not been studied. Insufflation of the ET by applying positive pressure to the ET orifice through the nasal cavity (Politzer maneuver) can temporarily relieve negative middle ear pressure, but these efforts are impractical for long-term benefit. Politzer devices for office or home use are available by prescription. Though not in widespread use, the technique of autoinflation has been used as a treatment for OME. The goal of autoinflation is to use either a Valsalva maneuver or external device to equalize middle ear and oropharyngeal pressure, essentially transiently opening the ET. One prospective cohort study found that adults with ETD following airplane travel had normalization of tympanometric pressures following use of a Politzer device for ET insufflation. A systematic review of six randomized trials found that Politzer devices are effective for treatment of OME in children; however, these trials did not assess other forms of ETD and did not evaluate adults.

MANAGEMENT Management of ETD in Active Chronic Otitis Media, Mucosal Disease The eustachian tube is dysfunctional due to inflammation, which has extended into the middle ear cleft also. In the active stage where there is copious pus discharge from the middle ear, a culture and sensitivity is done and the patient started on local as well as systemic antibiotics. The ear drops are applied twice daily, using the displacement technique, so that the patient is able to taste the applied ear drops, confirming ET patency. The treatment is continued for 7 days. In chronic ear discharge, only ear drops are used to control the discharge.

Video Feedback Tubo Therapy For moderate tubal dysfunction, it is possible to use video feedback tubo therapy for treatment. In this exercise, the TVPM and LVPM are strengthened and also, the patient is taught how to manage them and develop a better coordination. A micro fiberscope coupled with a camera is introduced through a nostril until the entrance of the ET is visualized. The patient is capable of acquiring sensation of his/her ET, called proprioception also on a separate tube. They will be able

26  Current Concepts of Otitis Media and Recent Management Strategies to face conditions at risk, such as during the diving. Therefore, we enable ET’s visualization in real time working by retroactive video feedback process.

Surgical Management A long-lasting dysfunction of the ET seems to be the etiologic origin for development of COM with mesotympanic perforation, OME and chronic atelectasis of the middle ear with or without cholesteatoma. Mastoidectomy, both canal wall-up and canal wall-down, can be used to treat persistent middle ear infection nor responding to the standard treatment or in patients have had repeated tympanoplasty, which have failed. However, these surgeries do not address the ETD.

Eustachian Tuboplasty Tuboplasty may be used in patients with chronic ETD with tympanic membrane atelectasis or middle ear effusion and who have undergone tympanostomy only to have grommets fall out on multiple occasions, while symptoms persist. It is done via nasal or transoral endoscopic approach. A laser or microdebrider is used to strip away hypertrophic mucosa and cartilage on the posterior ET cushion and into the valve area to clear obstruction. The valve is a 0.5 cm long region where mucosal surfaces from the anterior and posterior cushions are seen to oppose during tubal closure and dilate to the open position with normal tubal function. The reduction of the edematous mucosa and hypertrophied cartilage increases the concavity facing the TVPM and restores the lumen of the tube, which allows ventilation of middle ear during TVPM contraction. This allows TVP contraction to be more effective in opening the ET lumen. Eustachian tuboplasty may also be used to treat Patulus disease. The goal of these microendoscopic procedures is to restore the ET function by narrowing both tubal walls, avoiding intraluminal mucosal injury. This surgery is only slightly invasive and is mostly provided under general anesthesia. The approach is made through the nose and the mouth and leaves no injury or wound. Transposed LVPM brings forward cartilage and posterior wall to improve closure of the Patulous tubal channel. A mucosal vascularized flap is inserted in the anterior wall, above the TVPM in order to increase its bulging and anterior wall convexity. Inferior edge of the cartilage is shaped with laser. The LVPM is transposed back to close up, passively in steady state and actively when contracting, both tubal walls in order to narrow P tubal channel.

REFERENCES 1. Bluestone CD, Swarts JD. Human evolutionary history:consequences for the pathogenesis of otitis media. Otolaryngol Head Neck Surg. 2010;143(6):739-44. 2. Bluestone CD. Impact of evolution on the eustachian tube. Laryngoscope. 2008;118(3):522-7. 3. Sudo M, Sando I, Ikui A, et al. Narrowest (isthmus) portion of eustachian tube. a-computer-aided three-dimensional reconstruction and measurement study. Ann Otol Rhinol Laryngol. 1997;106(7 Pt 1):583-8.

Eustachian Tube and its Role in Otitis Media 27 4. Matsune S, Takahashi H, Sando I. Mucosa-associated lymphoid tissue in middle ear and Eustachian tube in children. Int J Pediatr Otorhinolaryngol. 1996;34(3):229-36. 5. Tos M, Bak-Pedersen K. Goblet cell population in the normal middle ear and Eustachian tube of children and adults. Ann Otol Rhinol Laryngol. 1976;85 (2 Suppl 25 Pt 2):44-50. 6. Johnson RM, Brown EJ. Cell-mediated immunity in host defense against infectious diseases. In: Mandell GL, Bennett JE, Dolin R (Eds). Principles and Practice of Infectious Disease, 5th edition. Philadelphia, Pa: Churchill Livingstone; 2000. pp.131-4. 7. Greer JP, Macon WR, McCurley TL. Non-Hodgkin lymphoma. In: Lee GR, Foerster J, Lukens J (Eds). Wintrobe’s Clinical Hematology, 10th edition. Baltimore, Md: Lippincott, Williams & Wilkins; 1999. pp. 2471-3. 8. Bufo P. The MALTomas. Academic lesson; 1999. 9. Kamimura M, Sando I, Balaban CD, et al. Mucosa-associated lymphoid tissue in middle ear and eustachian tube. Ann Otol Rhinol Laryngol. 2001;110(3):243-7. 10. Haginomori S, Balaban CD, Miura M, et al. Cellular proliferation of mucosaassociated lymphoid tissue with otitis media: a preliminary study. Ann Otol Rhinol Laryngol. 2002;111(10):926-32. 11. Ozturk K, Snyderman CH, Sando I. Do mucosal folds in the eustachian tube function as microturbinates? Laryngoscope. 2011;121(4):801-4. 12. Rapport PN, Lim DJ, Weiss HS. Surface-active agent in Eustachian tube function. Arch Otolaryngol. 1975;101(5):305-11. 13. Bluestone CD, Klein JO. Physiology, pathophysiology and pathogenesis. In: Bluestone CD, 2nd edn. Otitis media in infants and children. Philadelphia, PA: WB Saunders Co; 1988. pp.41-72. 14. Holmquist J. Eustachian tube anatomy and physiology. J Am Audiol Soc. 1977;2(4):115-20. 15. Ingelstedt S, Jonson B. Mechanism of the gas exchange in the normal human middle ear. Acta Otolaryngol. 1966;224:452-461. 16. Flisberg K. Ventilatory studies on the eustachian tube. A clinical investigation of cases with perforated ear drums. Acta Otolaryngol. 1966;(Suppl 219):1-82. 17. Thomsen KA. Investigations on the tuba1 function and measurement of the middle ear pressure in pressure chamber. Acta Otolaryngol Suppl. 1958;140:269-78. 18. Ingelstedt S, Ivarsson A Jonson B. Mechanics of the human middle ear. Pressure regulation in aviation and diving. A non-traumatic method. Acta Otolaryngol. 1967;(Suppl 228):1-58. 19. Al-Saab F, Manoukian JJ, Al-Sabah B, et al. Linking laryngopharyngeal reflux to otitis media with effusion: pepsinogen study of adenoid tissue and middle ear fluid. J Otolaryngol Head Neck Surg. 2008;37(4):565-71. 20. Bluestone CD. Assessment of eustachian tube function. In: Jerger J (Ed). Handbook of Clinical Impedance Audiometry. New York: American Electromedics Corp; 1975. pp.127-48. 21. Khan NA. Technique and clinical importance of eustachian tube radiography. Am J Otol. 1985;6(3):222-4. 22. Gaafar H, el Deeb AK, Abdel-Baki F et al. Flexible endoscopy and radiologic evaluation of the eustachian tube in adults with eustachian tube dysfunction. Am J Otol. 1988;9(5):357-62. 23. Kikuchi T, Oshima T, Ogura M, et al. Three-dimensional computed tomography imaging in the sitting position for the diagnosis of patulous eustachian tube. Otol Neurotol. 2007;28(2):199-203. 24. Takasaki K, Takahashi H, Miyamoto I, et al. Measurement of angle and length of the eustachian tube on computed tomography using the multiplanar reconstruction technique. Laryngoscope. 2007;117(7):1251-4.

28  Current Concepts of Otitis Media and Recent Management Strategies 25. Krombach GA, Nolte-Ernsting CC, Di Martino E, et al. Functional MRI of the eustachian tube in patients with clinical signs of dysfunction. Proc Intl Soc Mag Reson Med. 2001;9:89. 26. Linstrom CJ, Silverman CA, Rosen A, et al. Eustachian tube endoscopy in patients with chronic ear disease. Laryngoscope. 2000;110(11):1884-9. 27. Edelstein DR, Magnan J, Parisier SC, et al. Microfiberoptic evaluation of the middle ear cavity. Am J Otol. 1994;15(1):50-5. 28. Poe DS, Pyykko I, Valtonen H, et al. Analysis of eustachian tube function by video endoscopy. Am J Otol. 2000;21(5):602-7. 29. Poe DS. Endoscopic diagnosis of Eustachian tube dysfunction. In: Glasscock ME, Gulya AJ (Eds). Glasscock-Shambaugh. Surgery of the ear, 5th edition. Ontario, Canada: BC Decker Inc.; 2003. pp. 221-6. 30. Barsoumian R, Kuehn D, Moon JB, et al. An anatomic study of the tensor veli palatini and dilatator tubae muscles in relation to eustachian tube and velar function. Cleft Palate Craniofac J. 1998;35(2):101-10. 31. Mathew GA, Kuruvilla G, Job A. Dynamic slow motion video endoscopy in eustachian tube assessment. Am J Otolaryngol. 2007;28(2):91-7. 32. van Heerbeek N, Ingels KJ, Rijkers GT, et al. Therapeutic improvement of Eustachian tube function: a review. Clin Otolaryngol Allied Sci. 2002;27(1):50-6. 33. Seibert JW, Danner CJ. Eustachian tube function and the middle ear. Otolaryngol Clin North Am. 2006;39(6):1221-35. 34. Isaacson G, Buttaro GA, Mazeffa V, et al. Oxymetazoline solutions inhibit middle ear pathogens and are not ototoxic. Ann Otol Rhinol Laryngol. 2005;114(8):645-51.

4

Acute Otitis Media L Paul Emerson, Anand Job

INTRODUCTION Otitis media (OM) is divided into acute and chronic. Acute otitis media (AOM) is usually not life-threatening and is responsible for morbidities such as chronic otitis media (COM) and deafness that affects the quality of life and economic capability of both children and adults (Flow chart 1).

DEFINITIONS Acute otitis media is defined as an acute inflammatory process of the middle ear cleft.1,2 Recurrent AOM is defined as more than three AOM episodes during the previous 6 months or more than or equal to four AOM episodes during the previous 12 months.3,4 Nonresponsive AOM was defined as AOM occurring in less than or equal to 14 days after completing antibiotic treatment or not improving after more than or equal to 48 hours of therapy.5 Prevalence of AOM, in a cohort of 698 children followed, up to 3 years, 17% had three or more episodes by 1 year and 46% had three or more episodes by age of 3 years. Flow chart 1  Outcomes of acute otitis media

Abbreviations: CSOM, chronic suppurative otitis media; OME, otitis media with effusion

30  Current Concepts of Otitis Media and Recent Management Strategies

CLINICAL DIAGNOSIS Diagnosis of Acute Otitis Media A diagnosis of AOM requires:6 • History of acute onset of signs and symptoms • Presence of middle ear effusion (MEE) • Signs and symptoms of middle ear inflammation.

Elements of Acute Otitis Media Elements of the definition of AOM are as follows: • Recent, usually abrupt onset of signs and symptoms of middle ear inflammation and MEE • The presence of MEE indicated by any of the following:7,8 – Bulging of the tympanic membrane – Limited or absent mobility of the tympanic membrane – Air fluid level behind the tympanic membrane – Otorrhea through perforated tympanic membrane. • Signs or symptoms of middle ear inflammation as indicated by either: – Distinct erythema of the tympanic membrane or – Distinct otalgia that results in interference with or precludes normal activity or sleep.9 Children with AOM, usually present with a history of rapid onset of signs and symptoms such as otalgia (pulling of the ear in an infant), irritability (in an infant or toddler), otorrhea and/or fever. It should be noted that this presentation, other than otorrhea, is nonspecific and frequently overlaps those of a viral upper respiratory infection (URI). Other symptoms of a viral URI such as cough and nasal discharge or stuffiness, often precede or accompany AOM.

Eustachian Tube in Acute Otitis Media Obstruction of the eustachian tube (ET) is a key event associated with AOM. The vast majority of AOM episodes are triggered by an URI. ET obstruction is an important antecedent event in the development of AOM. Allergic and other inflammatory conditions involving the ET can lead to a similar outcome. Pathogenic bacteria in the nasopharynx colonize the normally sterile middle ear space through direct extension, aspiration or active insufflations. Inflammation in the nasopharynx extends to the medial end of the ET resulting in edema of the medial end of the ET, which, in turn, alters the pressure within the middle ear. Stasis resulting from ET obstruction and inflammation of the middle ear also allows the establishment of an acute inflammatory reaction characterized by vasodilatation, exudation, leukocyte invasion, phagocytosis and local immunologic responses within the middle ear cleft resulting in the clinical pattern of AOM.10,11 In a minority of otitis-prone children, the ET is found to be patulous or hypotonic. Also, children with neuromuscular disorders or abnormalities of the first or second arch are predisposed to reflux of nasopharyngeal contents into the middle ear cleft.

Acute Otitis Media 31

Mucosal Damage To become pathogenic in the ear or sinus, most bacteria must adhere to the mucosal lining. Viral infections that attack and damage mucosal linings of respiratory tracts may facilitate the ability of the bacteria to become pathogenic in the nasopharynx, ET and middle ear cleft. Mucosal damage by endotoxins secreted by bacteria may similarly enhance the adhesion of pathogens to mucosal surfaces.

Microbiology of Acute Otitis Media Pathogens The three most common pathogens causing otitis media are: 1. Streptococcus pneumoniae. 2. Hemophilus influenzae (typable and nontypable). 3. Moraxella catarrhalis. These are the main pathogens causing AOM.12 Group A streptococcus, which was a leading cause in the preantibiotic era, now contributes to less than 5% and occurs most often in school going children. In areas where there is widespread pneumococcal and Hib vaccination, nonvaccine serotypes of S. pneumoniae and nontypable H. influenzae are emerging as the leading pathogens. Viruses also contribute to AOM either alone or in combination with bacterial pathogens. The most common viruses isolated are respiratory syncytial virus, parainfluenza virus (types 1,2 and 3), influenza (A and B), enterovirus and rhinovirus.

Predictors of Acute Otitis Media Otitis media is common in children and several risk factors have been identified of which the most consistent ones are young age, with upper respiratory infections and family history. Less consistently, race, lack of breastfeeding, cigarette smoke exposure and pacifier use have been implicated. (Pediatric infectious diseases Long SS, Pickering LK, Prober CG 2008). Some children are prone to develop recurrent OM (four or more) in the 1st year of life. This could represent 5–10% of the general population. Various factors have been ascribed. Early nasopharyngeal colonization with the three major pathogens is associated with early first episode of AOM. Also, colonization has a direct bearing on the frequency of AOM. It has been noted that with mere colonization with S. pneumoniae or H. influenzae in the 1st year of life, the risk of having otitis increases four fold compared to those who are not colonized with a lower risk for M. catarrhalis. Rising air pollution could also contribute to OM.13 There were significant increases in prevalence of nonallergic respiratory illnesses like bronchitis, frequent colds, sinusitis, cough and decreased lung function in children from polluted areas.14 Evidence suggests that sulfur dioxide, nitrogen dioxide (NO2) and total suspended particles may be responsible.15 Exposure to these pollutants may result in a more severe or persistent infection by decreasing mucociliary clearance making progression to OM more likely.

32  Current Concepts of Otitis Media and Recent Management Strategies

Risk of Early Exposure to Pathogens It has been hypothesized that early exposure to multiple pathogens before maturation of the immune system results in partial immune tolerance or suppression and prolonged bacterial carriage, which leads to the persistence of OM as seen in a study done on aboriginal children. Early onset of OM (prior to age of 12 months) also results in lack of recovery from or recurrence of OM within 2 months. Once the tympanic membrane got perforated, it failed to heal as was observed on follow-up visits.

CONTRIBUTION OF ACUTE OTITIS MEDIA TO CHRONIC OTITIS MEDIA Many studies have established the link between early onset of OM, frequent/ recurrent OM and asymptomatic AOM for the progression to COM. This relationship suggests that interventions like antibiotics, vaccines to prevent early nasopharyngeal bacterial colonization, correct feeding practices, improved socioeconomic factors such as alleviation of poverty and improved housing with reduction of overcrowding, is likely to have a sustained impact.

Treatment of Acute Otitis Media (Table 1)16–19 Mild infection Healthy children with mild symptoms are kept under observation. Oral antibiotics are recommended in all children younger than 6 months and for those between 6 months, and 2 years with definitive diagnosis with standard-dose amoxicillin (40–45 mg/kg/day), when there are no complications.

Severe Infection For children with severe infection (moderate to severe otalgia or temperature of 39° Celsius or higher), those treated recently with antibiotic and for children who have been kept under observation and progressed, high-dosage amoxicillin (80–90 mg/kg/day) is recommended as first-line therapy. Macrolide antibiotics, clindamycin and cephalosporins are alternatives in penicillin-sensitive children.

Resistant Infection Patients who do not respond to treatment within 72 hours should be reassessed and high-dose amoxicillin clavulanate is preferred for treatment for patients with severe illness and in whom there is significant concern for β-lactamase-positive H. influenzae, drug resistant S. pneumoniae or M. catarrhalis or for patients who do not respond to amoxicillin within 72 hours.20

Follow-up Hearing and language testing is recommended in children with suspected hearing loss or persistent effusion for at least 3 months and in those with developmental problems. Rarely, myringotomy may need to be performed in AOM.

Acute Otitis Media 33 Table 1  First-line treatment in case of acute otitis media21 Initial antibiotic treatment

Antibiotic change after 48–72 hours of failed treatment

Recommended firstline treatment

Alternative treatment for penicillin allergy

Recommended firstline treatment

Alternative treatment

Amoxicillin (80–90 mg/kg/day in two divided doses)

Cefdinir (14 mg/kg/ day in 1–2 doses)

Amoxicillinclavulanatea (90 mg/ kg/day of amoxicillin, with 6.4 mg/kg day of clavulanate in two divided doses)

Ceftriaxone, 3 day Clindamycin (30–40 mg/kg/day in three divided doses), with or without third-generation cephalosporin

Amoxicillinclavulanatea (90 mg/ kg/day of amoxicillin, with 6.4 mg/kg/ day of clavulanate [amoxicillin to clavulanate ratio, 14:1] in two divided doses)

Cefuroxime (30 mg/ kg/day in two divided doses) Cefpodoxime (10 mg/ kg/day in two divided doses) Ceftriaxone (50 mg/ IM or IV/day/1–3 dose)

Ceftriaxone (50 mg IM or IV for 3 day)

Clindamycin (30–40 mg/kg/day in three divided doses) plus third-generation cephalosporin

Abbreviations: IM, intramuscular; IV, intravenous a  May be considered in patients who have received amoxicillin in the previous 30 days or who have the otitis-conjunctivitis syndrome

Indications of myringotomy/ventilation tubes22 are as follows: • Suppurative complication associated with AOM such as labyrinthitis, mastoiditis and facial palsy, when a ventilation tube also is needed • Severe otalgia23 • In tympanocentesis, for identification of organism in AOM in neonates and in immunocompromised status • Failure of antimicrobial prophylaxis in recurrent AOM.

Acute Otitis Media in Human Immunodeficiency Virus Acute otitis media is one of the most common infections that are implicated as significant contributors to morbidity in human immunodeficiency virus (HIV)infected children. OM prevalence in HIV-positive children may reach 80%,24 and the seropositive child is more prone to have the disease (and in a higher degree of severity), when compared to immunocompetent children. Moreover, for the HIV-immunocompromised, potential complications secondary to the disease affecting the middle ear such as otomastoiditis and central nervous system involvement must be considered. In HIV-infected children with absent or moderate immunosuppression, empiric antibiotic therapy should be based on the recommendations given for immunocompetent children of the same geographic area. In severe immunosuppressed stages, given the possible role of Staphylococcus aureus, extended spectrum antibiotics should be considered.

34  Current Concepts of Otitis Media and Recent Management Strategies

CONCLUSION To prevent COM, it is important to adequately treat AOM, so that progression to COM does not occur. Also, various strategies should be adopted to prevent AOM, so that ultimately the burden of COM is reduced.

REFERENCES 1. Bluestone CD. Definitions, terminology, and classification. In: Rosenfeld RM, Bluestone CD, (Eds). Evidence-based Otitis Media. Hamilton:BC Decker; 2003.pp. 120-35. 2. Bluestone CD, Klein JO. Definitions, terminology, and classification. In: Bluestone CD, Klein JO, (Eds). Otitis Media in Infants and Children, 4th edition. Hamilton: BC Decker; 2007. pp. 1-19. 3. Dowell SF, Marcy MS, Phillips WR, et al. Otitis media: principles of judicious use of antimicrobial agents. Pediatrics. 1998;101(suppl):165-71. 4. Rosenfeld RM. Clinical pathway for acute otitis media. In: Rosenfeld RM, Bluestone CD, (Eds). Evidence-based otitis media 2nd edition. Hamilton: BC Decker; 2003. pp. 280-302. 5. Leibovitz E, Piglansky L, Raiz S, et al. Bacteriologic and clinical efficacy of one day vs. three day intramuscular ceftriaxone for treatment of nonresponsive acute otitis media in children. Pediatr Infect Dis J. 2000;19(11):1040-5. 6. American Academy of Pediatrics Subcommittee on Management of Acute Otitis Media. Diagnosis and management of acute otitis media. Pediatrics. 2004;113(5):1451-65. 7. Hoberman A, Paradise JL, Rockette HE, et al. Treatment of acute otitis media in children under 2 years of age. N Engl J Med. 2011;364(2):105-15. 8. Tähtinen PA, Laine MK, Huovinen P, et al. A placebo controlled trial of antimicrobial treatment for acute otitis media. N Engl J Med. 2011;364(2):116-26. 9. Hayden GF, Schwartz RH. Characteristics of earache among children with acute otitis media. Am J Dis Child. 1985;139(7):721-3. 10. Klein JO, Bluestone CD. Otitis media. In: Feigin RD, Cherry JD, Demmler-Harrison GJ, (Eds). Textbook of Pediatric Infectious Diseases, 6th edn. Philadelphia, PA: Saunders; 2009.pp.216-37. 11. Chonmaitree T, Revai K, Grady JJ, et al. Viral upper respiratory tract infection and otitis media complication in young children. Clin Infect Dis. 2008;46(6):815-23. 12. Chonmaitree T, Heikkinen T. Role of viruses in middle-ear disease. Ann N Y Acad Sci. 1997;830:143-57. 13. Heinrich J, Raghuyamshi VS. Air pollution and otitis media: a review of evidence from epidemiologic studies. Curr Allergy Asthma Rep. 2004;4(4):302-9. 14. Frye C, Hoelscher B, Cyrys J, et al. Association of lung function with declining ambient air pollution. Environ Health Perspect. 2003;111(3):383-7. 15. Chauhan AJ, Inskip HM, Linaker CH, et al. Exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children. Lancet. 2003;361(9373):1939-44. 16. Hoberman A, Paradise JL, Burch DJ, et al. Equivalent efficacy and reduced occurrence of diarrhea from a new formulation of amoxicillin/clavulanate potassium (Augmentin) for treatment of acute otitis media in children. Pediatr Infect Dis J. 1997;16(5):463-70. 17. Arguedas A, Dagan R, Leibovitz E, et al. A multicenter, open label, double tympanocentesis study of high dose cefdinir in children with acuteotitis media at high-risk of persistent or recurrent infection. Pediatr Infect Dis J. 2006;25(3):211-8.

Acute Otitis Media 35 18. Atanaskovic-Markovic M, Velickovic TC, et al. Immediate allergic reactions to cephalosporins and penicillins and their cross-reactivity in children. Pediatr Allergy Immunol. 2005;16(4):341-7. 19. Pichichero ME. Use of selected cephalosporins in penicillin-allergic patients: a paradigm shift. Diagn Microbiol Infect Dis. 2007;57(3 Suppl):13S-18S. 20. Oral Update on the Role of Antibiotics in Children Less than 2 Years of Age with Acute Otitis Media. Yang Wang, Posted: 03/23/2011; Access Medicine from McGraw-Hill © 2011. The McGraw-Hill Companies. 21. Tunkel E, Rosenfeld M, Sevilla XD, Schwartz RH, Thoman PA, Hoberman DA, et al. The Diagnosis and Management of Acute Otitis Media. Pediatrics. 2013;131(3). 22. Bluestone CD. Eustachian Tube: Structure, Function, Role in Otitis Media. Hamilton Ontario, BC Decker Inc. 2005. 23. Roddey OF Jr, Earle R Jr, Haggerty R. Myringotomy in Acute Otitis Media. A Controlled Study JAMA. 1966;197(11):849-53. 24. Williams MA. Head and neck findings in pediatric acquired immune deficiency syndrome. Laryngoscope. 1987;97(6):713-6.

5

Chronic Otitis Media Associated with Effusion L Paul Emerson, Anand Job, John Mathew

INTRODUCTION Otitis media (OM) is one of the most common illness for which children visit a physician, receive antibiotics or undergo surgery. Chronic otitis media (COM) by definition is when there is inflammation in the middle ear for more than 3 months and an intact drum with middle ear effusion is known as chronic otitis media with effusion (COME) (Flow chart 1).1-3 The COME can result in conductive hearing loss,1 which has been linked to the delayed development of speech and socialization skills.4 Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis have been isolated from approximately 25% of children with COME and polymerase chain reaction (PCR)-based methods have demonstrated sequence-specific DNA and RNA for these pathogens in nearly 80% of cases (Figs 1 and 2). Other pathogenic factors associated with otitis media with effusion (OME) are recurrent viral upper respiratory infections, Eustachian tube dysfunction with impaired gas exchange, genetically predisposed host, persistent inflammatory mediators or exacerbation by gastroesophageal reflux (Figs 3 and 4).5,6 Another factor associated with COME is presence of ‘biofilms’, which explains the lack of antibiotic efficacy for this disorder.7-12 This resistance may stem from Flow chart 1  Various factors leading to otitis media

(Source: Bluestone CD, Klein JO. Physiology and pathogenesis. In: Bluestone CD, 2nd edn. Otitis media in infants and children. Philadelphia, PA: WB Saunders Co.; 1988.pp.41-72.)

Chronic Otitis Media Associated with Effusion  37

Fig. 1  Streptococcus pneumoniae

Fig. 2  Streptococcus pneumoniae pathogen with significant disease burden in children in United States (Source: Edwards KM, Pneumococcal infections: Therapeutic strategies and pitfalls in the Pneumococcus. (2004) ASM Press. Washington DC)

the fact that oxygen and nutrient limitation within biofilms induces metabolic quiescence, which in turn reduces antibiotic effectiveness.7 Other evidence suggests that biofilm bacteria may have genetic mechanisms, selected for in the biofilm, that provide antimicrobial protection.13-15 In addition, the biofilm provides a physical barrier that enhances pathogen resistance to host defenses such as opsonization, lysis by complement and phagocytosis (Fig. 5).16 The role of biofilms in the persistence of chronic mucosal-based, ear nose throat (ENT) related infections were first recognized in OM17 and adenotonsillitis.18 The size of the adenoid is not the main determinant factor in OME pathogenesis,

38  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 3  Acute mastoiditis

Fig. 4  Mechanism of infection of mastoid cavity through nasopharynx

but the degree of bacterial colonization is much more important.19 Adenoids in COME may act as a reservoir of chronic infection rather than causing mechanical eustachian obstruction. In adenoids, higher grade biofilm formation was found in cases with middle ear effusion than those with hypertrophy only. These findings support the hypothesis that there could be an association between adenoidal biofilm formation and COME. The efficacy of adenotonsillectomy on OME has been demonstrated by several randomized and controlled studies. Patients suffering from recurrent

Chronic Otitis Media Associated with Effusion  39

Fig. 5  Biofilm development cycle7-12

or chronic OME may benefit from adenoidectomy due to the removal of an infectious source in the nasopharynx rather than the removal of a large adenoidal mass.19 Adenoidectomy combined with grommet insertion provides improved benefit than only adenoidectomy alone.20 Chronic otitis media can occur from an unresolved or complicated acute otitis media (AOM) with perforation or from a pre-existing tympanic membrane perforation that either occurred spontaneously or from a prior pressure equalizing (PE) tube. Post-tympanostomy tube otorrhea (PTTO) is defined as active drainage through an existing PE tube.

CLASSIFICATION OF POST-TYMPANOSTOMY TUBE OTORRHEA Based on a recent meta-analysis by Rosenfeld,21 the following classification has been proposed to describe PTTO: • Early PTTO is that which occurs less than 2 weeks postoperatively. The reported incidences in the literature range between 5% and 49%. • Late PTTO occurs greater than 2 weeks postoperatively and is usually caused by pathologies similar to those responsible for AOM or from external contamination. • Chronic PTTO refers to otorrhea lasting greater than 8 weeks’ duration. • Recurrent PTTO refers to distinct episodes with clearing in between.

Prevention of Tympanostomy Tube Otorrhea Early Onset Approximately 10–20% of children who undergo placement of tympanostomy tubes develop otorrhea during the early postoperative period.22 The relative risk of early postoperative otorrhea is increased among children younger than 2 years of age and children with inflamed middle-ear mucosa, mucoid effusion,

40  Current Concepts of Otitis Media and Recent Management Strategies and bacterial pathogens in the ear canal or middle-ear effusion at the time of surgery. The administration of prophylactic eardrops during the postoperative period may decrease the incidence of early otorrhea and tube occlusion. It is independent of the eardrop used (e.g. saline, antibiotic eardrop with or without steroid, oxymetazoline, sulfacetamide-prednisolone eyedrops).23-28

Late Onset Prevention of recurrent tympanostomy tube otorrhea (TTO) in young children during the winter months involves the same measures used to control recurrent AOM in infants and young children. Oral or parenteral antimicrobial therapy is suggested for acute TTO in infants and children with systemic infection or edema of the auditory canal and for children with TTO who are immunocompromised. High dose amoxicillin (75–100 mg/kg/day, divided twice daily) or amoxicillin-clavulanate (with high dose amoxicillin) is suggested as empiric therapy.29 Topical antimicrobial therapy for acute TTO in immune-competent infants and children without systemic symptoms, occlusion of the auditory canal, or auricular cellulitis is suggested. Observation is also an option for such patient’s since many of these episodes resolve spontaneously. The use of a corticosteroidcontaining antibiotic drop is suggested when treating acute TTO with topical therapy. The addition of a corticosteroid to the antibiotic preparation helps to control granulation tissue involving the tympanic membrane and middle ear.30 Combination of systemic and topical therapy for children with acute TTO and associated auricular cellulitis is suggested. If the child fails to respond with resolution of visible otorrhea within 5 days, we suggest the addition of an antibiotic eardrop with activity against Pseudomonas aeruginosa and Staphylococcus aureus. The ear canal should be cleaned and the discharge sent for culture and sensitivities. Placing a porous wick in the inflamed ear canal may facilitate entry of the ototopical drop if the canal is occluded by secondary otitis externa.

Prevention Avoid water entering the ears.

Chronic Tympanostomy Tube Otorrhea Chronic TTO develops in approximately 4% of patients after placement of tympanostomy tubes.31 Prolonged use of any topical antimicrobial, particularly broad-spectrum fluoroquinolones may result in fungal overgrowth. Community-acquired methicillin-resistant S. aureus (CA-MRSA) and multiple-drug-resistant Streptococcus pneumoniae are other potential causes of TTO refractory to the usual antimicrobial therapy described above.32,33 It is recommended to obtained bacterial culture and sensitivities of the puru­ lent drainage in the ear canal in cases of refractory otorrhea; most laboratories report common fungi on routine culture. Culture is particularly important for detection of resistant organisms (e.g. CA-MRSA) or fungal overgrowth after

Chronic Otitis Media Associated with Effusion  41 prolonged antibiotic therapy. We recommend that antimicrobial therapy for refractory otorrhea should be based on culture and susceptibility results. Evaluation for possible immune deficiency may be warranted in children with TTO caused by unusual pathogens. Removing a tympanostomy tube is occasionally necessary to stop refractory otorrhea. Bacterial biofilms can form on mucosal surfaces and implanted prostheses, including tympanostomy tubes.

CONCLUSION Otitis media (OM) is one of the most common illnesses in children requiring medical and surgical management. Surgical management adenoidectomy combined with grommet insertion provides improved benefit. Early PTTO is a common, treatable entity, whereas chronic PTTO is not as common but is very problematic due to the formation of biofilms. Choice of PE tube surface characteristics may affect the incidence of PTTO with ionized treated PE tubes potentially being the most resistant to biofilm formation. Prophylactic use of antimicrobial drops may reduce early PTTO.

REFERENCES 1. Bluestone CD. Definitions, Terminology and Classification. In: Rosenfeld RM, Bluestone CD (Eds). Evidence based otitis media, 2nd edition. Ontario: BC Decker Inc; 2003. pp. 120-35. 2. Mahmood Bhutta, Steve Brown, Martin Burton. The Association of Chronic Otitis Media with Effusion (COME) and Recurrent Acute Otitis Media (RAOM) in UK Hospital Populations with the Genetic Loci Fbxo11 and Evi1. 3. Kubba H, Pearson JP, Birchall JP. The aetiology of otitis media with effusion: a review. Clin Otolarngol Allied Sci. 2000;25(3):181-94. 4. Bennett KE, Haggard MP, Silva PA, et al. Behaviour and developmental effects of otitis media with effusion into the teens. Arch Dis Child. 2001;85(2):91-5. 5. Takahashi H. The Middle Ear: The Role of Ventilation in Disease and Surgery. Tokyo: Springer-Verlag; 2001. 6. Neto JFL, Hemb L, Silva DB. Systematic literature review of modifiable risk factors for recurrent acute otitis media in childhood. J Pediatr (Rio J). 2006;82(2):87-96. 7. Borriello G, Werner E, Roe F, et al. Oxygen limitation contributes to antibiotic tolerance of Pseudomonas aeruginosa in biofilms. Antimicrob Agents Chemother. 2004;48(7):2659-64. 8. Roberts ME, Stewart PS. Modelling protection from antimicrobial agents in biofilms through the formation of persister cells. Microbiology. 2005;151(Pt 1):75-80. 9. Anderl JN, Zahller J, Roe F, et al. Role of nutrient limitation and stationary-phase existence in Klebsiella pneumoniae biofilm resistance to ampicillin and ciprofloxacin. Antimicrob Agents Chemother. 2003;47(4):1251-6. 10. Fux CA, Wilson S, Stoodley P. Detachment characteristics and oxacillin resistance of Staphyloccocus aureus biofilm emboli in an in vitro catheter infection model. J Bacteriol. 2004;186(14):4486-91. 11. Stewart PS, Costerton JW. Antibiotic resistance of bacteria in biofilms. Lancet. 2001;358(9276):135-8. 12. Post JC, Preston RA, Aul JJ, et al. Molecular analysis of bacterial pathogens in otitis media with effusion. JAMA. 1995;273(20):1598-604. 13. Mah TF, Pitts B, Pellock B, et al. A genetic basis for Pseudomonas aeruginosa biofilm antibiotic resistance. Nature. 2003;426(6964):306-10.

42  Current Concepts of Otitis Media and Recent Management Strategies 14. Drenkard E, Ausubel FM. Pseudomonas biofilm formation and antibiotic resistance are linked to phenotypic variation. Nature. 2002;416(6882):740-3. 15. Christensen BB, Sternberg C, Andersen JB, et al. Establishment of new genetic traits in a microbial biofilm community. Appl Environ Microbiol. 1998;64(6):2247-55. 16. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science. 1999;284(5418):1318-22. 17. Post JC, Hiller NL, Nistico L, et al. The role of biofilms in otolaryngologic infections: update 2007. Curr Opin Otolaryngol Head Neck Surg. 2007;15(5):347-51. 18. Galli J, Calò L, Ardito F. Biofilm formation by Haemophilus influenzae isolated from adeno-tonsil tissue samples, and its role in recurrent adenotonsillitis. Acta Otorhinolaryngol Ital. 2007;27(3):134-8. 19. Park K. Otitis Media and Tonsils – Role of adenoidectomy in the treatment of chronic otitis media with effusion. In: Harabuchi Y (Ed). Recent Advances in Tonsils and Mucosal Barriers of the Upper Airways. Adv Otorhinolaryngol Ital. Basel: Karger; 2011. pp. 160-3. 20. Bluestone CD. Eustachian Tube: Structure, Function, Role in Otitis Media. Ontario, Canada: BC Decker 1989;160(1):83-94. 21. Rosenfeld RM. Surgical prevention of otitis media. Vaccine. 2000;19:S134-9. 22. Kay DJ, Nelson M, Rosenfeld RM. Meta-analysis of tympanostomy tube sequelae. Otolaryngol Head Neck Surg. 2001;124(4):374-80. 23. Poetker DM, Lindstrom DR, Patel NJ, et al. Ofloxacin otic drops vs neomycinpolymyxin B otic drops as prophylaxis against early postoperative tympanostomy tube otorrhea. Arch Otolaryngol Head Neck Surg. 2006;132(12):1294-8. 24. Kumar VV, Gaughan J, Isaacson G, et al. Oxymetazoline is equivalent to ciprofloxacin in preventing postoperative otorrhea or tympanostomy tube obstruction. Laryngoscope. 2005;115(2):363-5. 25. Kocaturk S, Yardimci S, Yildirim A, et al. Preventive therapy for postoperative purulent otorrhea after ventilation tube insertion. Am J Otolaryngol. 2005;26(2):123-7. 26. Morpeth JF, Bent JP, Watson T. A comparison of cortisporin and ciprofloxacin otic drops as prophylaxis against post-tympanostomy otorrhea. Int J Pediatr Otorhinolaryngol. 2001;61(2):99-104. 27. Charnock DR. Early postoperative otorrhea after tympanostomy tube placement: a comparison of topical ophthalmic and otic drops. Ear Nose Throat J. 1997;76(12):870-1. 28. Hester TO, Jones RO, Archer SM, et al. Prophylactic antibiotic drops after tympanostomy tube placement. Arch Otolaryngol Head Neck Surg. 1995;121(4): 445-8. 29. Ruohola A, Heikkinen T, Meurman O, et al. Antibiotic treatment of acute otorrhea through tympanostomy tube: randomized double-blind placebo-controlled study with daily follow-up. Pediatrics. 2003;111(5 Pt 1):1061-7. 30. Roland PS, Dohar JE, Lanier BJ, et al. Topical ciprofloxacin/dexamethasone otic suspension is superior to ofloxacin otic solution in the treatment of granulation tissue in children with acute otitis media with otorrhea through tympanostomy tubes. Otolaryngol Head Neck Surg. 2004;130(6):736-41. 31. Kay DJ, Nelson M, Rosenfeld RM. Meta-analysis of tympanostomy tube sequelae. Otolaryngol Head Neck Surg. 2001;124(4):374-80. 32. Al-Shawwa BA, Wegner D. Trimethoprim-sulfamethoxazole plus topical antibiotics as therapy for acute otitis media with otorrhea caused by community-acquired methicillin-resistant Staphylococcus aureus in children. Arch Otolaryngol Head Neck Surg. 2005;131(9):782-4. 33. Hwang JH, Tsai HY, Liu TC. Community-acquired methicillin-resistant Staphylococcus aureus infections in discharging ears. Acta Otolaryngol. 2002;122(8):827-30.

6

Chronic Otitis Media L Paul Emerson, Anand Job

INTRODUCTION Chronic suppurative otitis media (CSOM), its classification and definition have undergone much change. The CSOM traditionally has been classified as safe or tubotympanic disease (TTD), i.e. disease in the mesotympanum, hypotympanum and eustachian tube and unsafe, i.e. disease in the attic and antrum/mastoid, also known as atticoantral disease (AAD). In CSOM, TTD, there is a perforation of the pars tensa with mucopurulent discharge. In CSOM, AAD there is an attic perforation or posterosuperior retraction pocket with cholesteatoma/ granulations and pus. This classification based on the term CSOM, has been replaced by chronic otitis media (COM). The term COM implies an abnormality of the pars tensa/pars flaccida as a result of acute otitis media, negative middle ear pressure or otitis media with effusion. There may or may not be a perforation of the TM. It can be subdivided into COM, mucosal disease and COM, squamosal disease.

Active Mucosal Chronic Otitis Media The middle ear mucosa shows chronic inflammation with edema, submucosal fibrosis and increased vascularity. The mucosa can ulcerate in certain areas with formation of granulation tissue. There is a permanent perforation of the pars tensa with intermittent discharge. The middle ear mucosa may undergo polypoidal changes causing ‘aural polyp’. The inflammatory changes are not confined to the middle ear alone and the whole of the middle ear cleft may be involved. Often there is associated resorption of parts or whole of ossicular chain. This could be due to resorptive osteitis. The ossicles affected typically show hyperemia with proliferation of capillaries and prominent histiocytes. Long process of incus is commonly eroded, followed by stapes crurae, body of incus and manubrium in that order. The proposed mechanism of erosion in chronic middle ear inflammation is as a result of overproduction of interleukin-2, fibroblast growth factor and platelet derived growth factor, which promote hyper vascularization, osteoclast activation and bone resorption causing ossicular damage. Tumor necrosis factoralpha (TNF-α) also produces neovascularization and hence, granulation tissue formation. COM is thus an inflammatory process with a defective wound healing mechanism. This inflammatory process in the middle ear is more harmful the longer it stays and the nearer it is to the ossicular chain. In some ears with active COM (mucosal and cholesteatomatous), areas of cholesterol granuloma are seen (Fig. 1). These granulomas have areas of giant

44  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 1  Active chronic otitis media

cell reaction around cholesterol crystals, can be present anywhere in the middle ear cleft and rarely become the dominant pathology. Cholesterol crystals are breakdown products of hemorrhage.

Inactive Mucosal Chronic Otitis Media There is permanent perforation of the pars tensa, with no inflammation of the middle ear cleft. The rim of the perforation is thickened due to proliferation of fibrous tissue. Although usually the mucocutaneous junction is at the margin of the perforation, at times, squamous epithelium can migrate medially onto the undersurface of the drum remnant and care should be taken to remove this epithelium completely, while performing tympanoplasty (Fig. 2).

Active Squamous Chronic Otitis Media (Fig. 3) This condition is otherwise known as unsafe ear or cholesteatoma. It is associated with retraction of pars flaccida/tensa (usually posterosuperiorly) that has retained squamous epithelial debris (cholesteatoma). There is also associated inflammation of middle ear cleft mucosa and submucosa with production of pus, and erosion of mastoid bone and ossicles. This condition leads to intracranial complications more frequently than mucosal COM due to resorption of bone, osteitis, granulations and persistent infection. Chronic mastoiditis may also be present.

Inactive Squamous Chronic Otitis Media In this condition, the middle ear mucosa and mastoid appear relatively healthy. Reactivation of disease can occur because of the existing pathology.

Chronic Otitis Media 45

Fig. 2  Dry central perforation of ear drum

Fig. 3  Active squamous chronic otitis media

These include retraction pockets, atelectasis and epidermization. Negative middle ear pressure can cause retraction of tympanic membrane (TM). A retrac­ tion pocket consists of an invagination into the middle ear space of part of the ear

46  Current Concepts of Otitis Media and Recent Management Strategies drum (pars flaccida or pars tensa). These retraction pockets may be fixed when it is adherent to structures in the middle ear or free when it can move freely medially or laterally depending on the state of inflation of the middle ear. ‘Epidermization’ denotes replacement of middle ear mucosa by keratinizing squamous epithelium without retention of keratin debris. The area of epidermization may involve part or the entire middle ear cavity. Epidermization often remain quiescent and does not progress to cholesteatoma or active suppuration. So epidermization per se is not an indication for surgical intervention.

Healed Chronic Otitis Media In this stage, the perforated ear drum has healed by itself. The lack of fibrous layer or due to absence or atrophy of the TM, leads to a ‘dimeric’ membrane that consists of epidermis and mucosa only. Such thin membrane is more prone to retraction, if there is negative middle ear pressure. Tympanosclerosis is also another form of healed ear drum. It refers to hyaline deposits of acellular material visible as whitish plaques in the TM or as white nodular deposits in the submucosal layers of the middle on otoscopy. Tympanosclerosis is the end result of a healing process in which collagen in fibrous tissue hyalinizes, loses its structure and become fused into a homogenous mass. Calcification and ossification also occur to a variable extent.

Fibrocystic and Fibro-osseous Sclerosis Sometimes in healed COM, fibrosis and cyst formation is seen. This obliterates large portions of the middle ear cleft. There is deposition of new bone resulting in a sclerotic mastoid. This can involve spaces around the ossicles such as the epitympanum causing conductive hearing loss. It is impossible to reverse these changes and surgery is most often a failure.

CONCLUSION Chronic otitis media (COM) is characterized by chronic inflammation of middle ear cleft with defective wound healing. Of recent it has been classified into mucosal and squamosal disease. Recurrent infections lead to mucosal ulceration, fibrosis and granulation tissue formation in the middle ear cleft leading to secondary complications. Very often, surgical management is the treatment of choice.

BIBLIOGRAPHY 1. Browning GG. Chapter 3. Etiopathology of inflammatory conditions of the external and middle ear. In: Kerr AG Scott Brown’s Otolaryngology, 6th edn. Vol. 3. London: Arnold; 1997. 2. Browning GG, et al. Chapter 237c chronic otitis media in Scott-Brown’s Otolaryngology, 7th edn. Vol. 3. London: Arnold; 2008.

7

Chronic Otitis Media-Mucosal Disease Anand Job, L Paul Emerson

INTRODUCTION Chronic otitis media-mucosal disease (COM-MD), was earlier known as chronic suppurative otitis media (CSOM) or tubotympanic disease. The usual history is that of intermittent ear discharge from the middle ear lasting more than 6–12 weeks.1,2 Occasionally, the epithelium undergoes change to squamous type forming cholesteatoma, and is known as COM, squamosal disease. COM-MD can at times be difficult to treat due to a variety of reasons.2

ETIOPATHOLOGY Chronic otitis media mucosal disease is initiated by an episode of acute otitis media or after recurrent acute otitis media. It begins as inflammation of the middle ear mucosa, causing mucosal edema and middle ear effusion, which becomes purulent, causing pressure necrosis of the tympanic membrane (TM) resulting in a central perforation of varying size. Sometimes, due to virulence of the organism or immunocompromised state of the host, necrotizing otitis media can develop, with total perforation and ossicular necrosis as well.3 If the patient is seen before this event, a myringotomy is done, which leads to a much smaller perforation allowing spontaneous healing. Reasons for spontaneously nonclosure are due to several factors such as formation of a fibrous ring around the edges of the perforation, recurrent infections and the presence of a large perforation. Due to the long standing perforation, it is also known as permanent perforation. Recurrent infections lead to mucosal ulceration, fibrosis and granulation tissue formation in the middle ear. Polyp formation can also occur, which when large; can prolapse into the external auditory canal. The granulation tissue eventually erodes the ossicles and destroys the surrounding bone and can lead to various complications of COM.

BACTERIOLOGY Pseudomonas aeruginosa, Staphylococcus aureus, Proteus, Klebsiella and Diphtheroids are the most common bacteria cultured from chronically draining ears. Anaerobes (Bacteroides, Peptostreptococcus, Peptococcus) and fungi (Aspergillus and Candida) have been cultured and found to grow concurrently and thought to cause an increase in virulence and persistence of the bacterial infection.4,5

48  Current Concepts of Otitis Media and Recent Management Strategies P. aeruginosa uses pili to attach to the diseased epithelium of the middle ear to produce proteases, lipopolysaccharide and other enzymes to prevent normal immunologic defense mechanisms from fighting the infection. The ensuing damage from bacterial and inflammatory enzymes causes continued damage, resulting in bony erosion.6 Current belief is that a continued infection of the middle ear cleft is related to translocation of bacteria from the external auditory canal through the perforation into the middle ear. Although some authors have suggested that pathogenic organisms may enter through Eustachian tube (ET), the data supporting this theory is inconclusive as most of the pathogenic bacteria are those common to the external auditory canal.

INVESTIGATIONS If unresponsive to medical treatment (with culture guided antibiotic treatment), a computed tomography (CT) scan of the temporal bone may reveal the presence of cholesteatoma/granulations in the mastoid. CT scan is useful to delineate anatomical structures such as facial canal, ossicles, sinus plate and tegmen as landmarks, if mastoidectomy is required, especially when congenital anomalies are present. CT scan is also helpful in the diagnosis of labyrinthine fistula and other otological and intracranial complications, which are less commonly seen today. A pure tone audiogram is done to know the degree of conductive hearing loss. Mild conductive hearing loss is usually associated with an intact ossicular chain and a small central perforation. In ossicular discontinuity and larger perforations, the conductive hearing loss approaches 50 dB and in more severe and mixed loss it indicates a more extensive disease involving the labyrinth or can be due to the inadvertent use of ototoxic medication such as gentamycin.

MEDICAL TREATMENT The aim of treatment is to achieve a dry ear so that either spontaneous closure may occur or tympanoplasty can be done so that hearing may be restored and recurrence of discharge can be prevented. Response to topical therapy is superior to systemic antibiotics as the local concentrations of ear drops reached are very high and overcome bacterial resistance also. Treatment consists of five important components: 1. Aural toilet 2. Selection of appropriate antibiotic drops 3. Managing granulations 4. Treating the ET 5. Dealing with nonotological factors that contribute to reinfections like allergic rhinitis, chronic sinusitis, adenotonsillitis.

Aural Toilet Unless the discharge is removed from the ear canal, topically preparations cannot penetrate the affected tissues. Aural toilet is best achieved using the microscope to suck out the tenacious mucopurulent exudates. Ideally, aural toilet should be performed 2–3 times/day prior to administration of ear drops.

Chronic Otitis Media-Mucosal Disease 49

Antibiotics Antibiotic ear drops prescribed should cover gram-negative organisms like Pseudomonas, Klebsiella and Proteus, and gram-positive organisms like S. aureus. Ciprofloxacin ear drops is a broad spectrum antibiotic and is ideal as it is nonototoxic as well, and well tolerated.

Antiseptic Ear Drops Povidone iodine (PVP-I) is nonototoxic and has been studied in COM with active disease and was found to be having an efficacy of 88% as compared to 90% for ciprofloxacin ear drops. The most commonly isolated organism was P. aeruginosa. In vitro resistance to ciprofloxacin was seen in 17% of organisms, while no resistance was seen for PVP-I. Also, there is an added benefit of reduced cost of therapy. The drops can be safely used from 10 days to 3 weeks.7

Drops that Lower the pH Level While low pH is an advantage when treating external otitis, in the middle ear (pH is neutral) pH lowering drops cause pain and irritation of the mucosa.

Viscosity Antibiotic ear drops solutions have low viscosity compared to preparations containing steroids, which have considerably higher viscosity. When combining antibiotics with steroids, the solution becomes more viscous than antibiotic alone and is more effective in coating and remaining in contact with the tissues for longer periods. The disadvantage is that it is less likely to move around the small spaces of the middle ear than low viscosity preparations.

Steroid-containing Drops The anti-inflammatory effect of steroids is significant when granulation tissue is present. Studies have shown that ototopicals with steroids are superior to steroid-free preparations in reducing granulation tissue at days 11 and 18 of treatment. In eosinophilic otitis media with resistant ear discharge, triamcinolone used as ear drops has been found to be very effective, proving the efficacy of steroid ear preparations.

Bacterial Resistance Studies have not identified any increase in bacterial resistance for ototopical antibiotics. It has been observed clinically that the concentration of quinolone ear drops overwhelms the most resistant of organisms.

Granulation Tissue Granulation tissue when present in the middle ear can cause persistence of infection. If no improvement is seen after using topical steroids, chemical cautery using silver nitrate is frequently used. Caution must be exercised, as the depth of

50  Current Concepts of Otitis Media and Recent Management Strategies burn is uncontrolled. Excision of granulation tissue can also be done using the microscope and microinstruments. Silver nitrate can be used as an adjunct to control bleeding and to enhance the efficacy of granulation tissue removal. Due caution should be exercised as the facial nerve could be exposed and fistula of the lateral semicircular canal may be present.

Eustachian Tube Patency While applying the ear drops, the patient should be lying down with the infected ear uppermost and after aural toilet, the drops are applied by the displacement method, ensuring a bitter taste in the mouth, signifying that the drops have gone through the ET, which promotes patency and therapy. Factors affecting spontaneous healing: • Size of perforation • Presence of discharge • Tympanosclerosis. Cauterize the edges of small perforation with silver nitrate also leads to healing.

REFERENCES 1. Matsuda Y, Kurita T, Ueda Y, et al. Effect of tympanic membrane perforation on middle-ear sound transmission. J Laryngol Otol Suppl. 2009;(31):81-9. 2. Wright D, Safranek S. Treatment of otitis media with perforated tympanic membrane. Am Fam Physician. 2009;79(8):650, 654. 3. Vikram BK, Khaja N, Udayashankar SG, et al. Clinico-epidemiological study of complicated and uncomplicated chronic suppurative otitis media. J Laryngol Otol. 2008;122(5):442-6. 4. Meyerhoff WL, Kim CS, Paparella MM. Pathology of chronic otitis media. Ann Otol Rhinol Laryngol. 1978;87(6 Pt 1):749-60. 5. Brobby GW, Zadik P. Bacteriology of otitis media in Ghana. Trop Doct. 1987;17(2): 91-2. 6. Browning GG, Gatehouse S, Calder IT. Medical management of active chronic otitis media: a controlled study. J Laryngol Otol. 1988;102(6):491-5. 7. Chronic suppurative otitis media. [online]. Website. Emedicine medscape available from emedicine.medscape.com/article/859501 [Accessed November, 2013].

8

Microbiology of Acute Otitis Media Shalini Anandan, L Paul Emerson, Anand Job

INTRODUCTION Acute otitis media (AOM) usually results as a complication of a viral upper respiratory tract infection, which causes a middle ear effusion, which can become infected secondarily with bacterial organisms found in the upper airway. These organisms could have been present in the upper respiratory tract either as pathogens or as colonizers.1 Various viruses have been isolated from middle ear effusions of 8–25% patients with otitis media. The viruses known to cause AOM are respiratory syncytial virus, influenza virus, adenovirus and rhinovirus.2 Culturing middle ear fluid samples from children with otitis media, results in the isolation of bacterial species in approximately 30–50% of the cases. Hemophilus influenzae, Streptococcus pneumoniae, Streptococcus pyogenes and Moraxella catarrhalis, are the classic middle ear pathogens of AOM. Several studies have suggested Alloiococcus otitidis as an additional pathogen as it is the most common isolated from the middle ear isolates in recent studies. 3 In a study of 70 healthy volunteers (aged 19–22 years) there was a high prevalence (> 80%) of A. otitidis in the outer ear in contrast to its absence in the nasopharynx. H. influenzae was found in both the outer ear and the nasopharynx (6% and 14%, respectively), whereas S. pneumoniae and M. catarrhalis were found only in the nasopharynx (9% and 34%, respectively). Hence, the role of A. otitidis remains ambiguous because middle ear infecting organisms are considered to invade the middle ear from the nasopharynx through the eustachian tube. Occasionally, Chlamydia pneumoniae has been isolated from the middle ear and this organism responds to macrolides. Although anaerobic bacteria such as Peptostreptococcus species, Bacteroides species, Fusobacterium species, Porphyromonas species and Prevotella species have been known to be recovered from middle ears of children with AOM, data does not support a significant role for this species and is usually isolated with other pathogens.4 It has been found worldwide that the type of organisms varies with age and region. In addition, the introduction of pneumococcal vaccines has reduced the number of S. pneumoniae causing otitis media in many regions depending on the prevalent serotype and the valency of the pneumococcal vaccine available in that region.5

52  Current Concepts of Otitis Media and Recent Management Strategies

Diagnosis When the tympanic membrane is perforated, drainage fluid may be available for gram staining and culture. Cultures of the nasopharynx are unreliable compared to culture of middle-ear aspirates for determination of the etiologic agents of otitis media.

Specimen Collection, Transport and Processing for Culture Drainage fluid can be collected from the external ear canal on swabs for culture with the help of a microscope. It is recommended that a second swab is collected as with any sample for microbiology, for Gram stain. Swabs if not processed within 2 hours, must be stored in room temperature in transport media such as Amie’s media. Samples for anaerobic culture should also be kept at room temperature until processing.

REFERENCES 1. Short KR, Reading PC, Brown LE, et al. Influenza-induced inflammation drives pneumococcal otitis media. Infect Immun. 2013;81(3):645-52. 2. Ruuskanen O, Arola M, Heikkinen T, et al. Viruses in acute otitis media: increasing evidence for clinical significance. Pediatr Infect Dis J. 1991;10(6):425-7. 3. Khoramrooz SS, Mirsalehian A, Emaneini M, et al. Frequency of Alloicoccus otitidis, Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae in children with otitis media with effusion (OME) in Iranian patients. Auris Nasus Larynx. 2012;39(4):369-73. 4. Brook I, Schwartz R. Anaerobic bacteria in acute otitis media. Acta Oto-laryngologica. 1981;91:1-6,111-4. 5. Alonso M, Marimon JM, Ercibengoa M, et al. Dynamics of Streptococcus pneumoniae serotypes causing acute otitis media isolated from children with spontaneous middle-ear drainage over a 12-year period (1999-2010) in a region of northern Spain. PLoS One. 2013;8(1):e54333.

9

Microbiology of Chronic Otitis Media Shalini Anandan, Anand Job, L Paul Emerson

INTRODUCTION Pseudomonas aeruginosa, Staphylococcus aureus, Proteus, Klebsiella pneumoniae, and diphtheroids are the most common bacteria cultured from chronically draining ears. Anaerobes and fungi may grow concurrently with the aerobes in a symbiotic relationship. The clinical significance of this relationship although unproven, is theorized to cause an increased virulence of the infection.1,2 Pseudomonas aeruginosa is the most commonly recovered organism from the chronically draining ear. Various researchers over the past few decades have recovered Pseudomonas from 48 to 98% of patients with chronic otitis media (COM). Pseudomonas aeruginosa uses pili to attach to necrotic or diseased epithelium of the middle ear. Once attached, the organism produce proteases, lipopolysaccharide and other enzymes to prevent normal immunologic defense mechanisms from fighting the infection. The ensuing damage from bacterial and inflammatory enzymes create further damage, necrosis and eventually, bony erosion leading to some of the complications seen in COM.3 Pseudomonal infections commonly resist macrolides, extended-spectrum penicillins and first and second generation cephalosporins. This can complicate treatment plans, especially in children. Staphylococcus aureus is the second most common organism isolated from chronically diseased middle ears. Reported data estimate infection rates from 15–30% of culture-positive draining ears. The remainder of infections is caused by a large variety of gram-negative organisms. Klebsiella (10–21%) and Proteus (10–15%) species are slightly more common than other gram-negative organisms. Polymicrobial infections are seen in 5–10% of cases, often demonstrating a combination of gram-negative organisms and S. aureus. The anaerobes (Bacteroides, Peptostreptococcus, Peptococcus) and fungi (Aspergillus, Candida) completes the spectrum of colonizing organisms responsible for this disease. The anaerobes make up 20–50% of the isolates in COM and tend to be associated more with cholesteatoma.

Role of Fungi in Chronic Otitis Media Many authors have focused their attention on the bacterial flora of chronic suppurative otitis media, but very little is known about the mycological aspects of fungi, the importance of which has been increasing in the recent years because

54  Current Concepts of Otitis Media and Recent Management Strategies of the excessive use of broad-spectrum antibiotics, corticosteroids and cytotoxic chemotherapy and an increase in the number of immune deficiency conditions. Prolonged use of broad-spectrum antibiotics and/or steroid ear drops may also cause suppression of the bacterial flora and the subsequent emergence of fungal flora. Candida albicans was found to be associated with bacteria in 66.7% of the cases and Aspergillus fumigatus and A. niger were associated with bacteria in 16.7% cases (each).4

REFERENCES 1. Brobby GW, Zadik P. Bacteriology of otitis media in Ghana. Trop Doct. 1987;17(2): 91-2. 2. Browning G, Gatehouse S, Calder T. Medical management of active chronic otitis media: a controlled study. J Laryngol Otol. 1988;102(6):491-5. 3. Chronic suppurative otitis media. [online] medscape website. Available from emedicine.medscape.com/article/859501[Accessed November 2013]. 4. Harvinder Kumar, Sonia Seth. Bacterial and Fungal Study of 100 Cases of Chronic Suppurative Otitis Media. J Clin Diagn Res. 2011;5:1224-7.

10

Pathophysiology of Chronic Otitis Media Anand Job, L Paul Emerson

INTRODUCTION It is accepted that chronic otitis media (COM) is preceded by acute otitis media (AOM), either untreated or treated incompletely or unsuccessfully.1-3 The pathophysiology of COM is initiated by middle ear inflammation causing mucosal edema, which can lead to formation of mucosal polyps which when large, can prolapse into the external auditory canal through an existing pars tensa perforation of the tympanic membrane (TM). The ongoing inflammation sometimes, can lead to mucosal ulceration and consequent breakdown of the epithelial lining. The host’s attempt at resolving the infection causing inflammation and ulceration manifests as granulation tissue, which can develop into a granulation polyp. The cycle of inflammation, ulceration, infection and granulation tissue formation may continue, eventually destroying the surrounding bony margins causing otitis with irreversible tissue damage and can lead to cholesteatoma formation and the various complications of COM. The normal lining of the middle ear cavity is pseudostratified columnar ciliated epithelium in its antero-inferior half to two-thirds, extending from the eustachian tube orifice, in three pathways to the: 1. Hypotympanum. 2. Promontory. 3. Anterior epitympanum.4 Ciliated epithelium has been shown to be morphologically identical to other types of respiratory lining, consisting of four cell types: 1. Ciliated. 2. Nonciliated cells with microvilli. 3. Secretory cells. 4. Basal cells. Shimada and Lim in 1972, studied the distribution of ciliated cells in normal middle ear mucosa and showed that the distribution and density of ciliated epithelial cells decreased in an anterior to posterior direction from over 80% of the total mucosal surface in the eustachian tube, to 11–50% in the remainder of the promontory, to 1–10% in the prominence of the facial canal and to less than 1% in the mastoid cavity.5 COM is associated with ciliary destruction more evident and marked in the cholesteatomatous type than in the mucosal type.6 The earliest morphological changes in middle ear inflammation involves the lamina propria, which shows an increased capillary permeability with edema and leukocytic infiltration. During the late acute to subacute stages, the mucosa shows a marked increase in numbers of ciliated and secretory epithelial cells.

56  Current Concepts of Otitis Media and Recent Management Strategies As the inflammatory process enters the chronic phase, there is a continuing shift in the population of infiltrating leukocytes toward increasing numbers of mononuclear cells that secrete substances that facilitate tissue destruction and fibrosis. There is also development and proliferation of granulation tissue, which is intimately involved in the process of bony erosion. As granulation tissue matures, it becomes denser and less vascular, a process that leads to fibrosis and formation of adhesions that may significantly compromise middle ear function.7 The mucosal polyp or granulation polyp can also block the middle ear mucosal spaces and communicating openings, preventing drainage of the mastoid antrum. Chronic obstruction of the attic and mastoid antrum with infection leads to irreversible changes in the mucosa and bone of the mastoid.

ROLE OF INFLAMMATORY MEDIATORS IN THE PATHOGENESIS OF OTITIS MEDIA AND THEIR SEQUELAE (FLOW CHART 1)8 The immune system responds to injury or irritation through an innate cascade known as inflammation. Central to the formation of inflammation are inflammatory mediators, which include proteins, peptides, glycoproteins, cytokines, arachidonic acid metabolites (prostaglandins and leukotrienes), nitric oxide and oxygen free radicals. These compounds are produced by epithelial cells, endothelial cells and infiltrating inflammatory cells. Inflammatory mediators are a double-edged sword, having the potential to fight off infection, but also to damage the host. In otitis media (OM), there is an inflammatory response to either acute or persistent stimuli, typified by the accumulation of both cellular and chemical mediators in the middle ear cleft.9 These mediators have a role in the inflammatory processes of the middle ear such as vascular permeability changes, chemotaxis, stimulation of epithelial secretory activity, enhancement of mucous glycoprotein secretion and production of other mediators.

Flow chart 1  Pathophysiology of chronic otitis media­18

Pathophysiology of Chronic Otitis Media 57

Initiation of Inflammation Endotoxin, a component of bacterial cell wall, is believed to be responsible for initiating inflammation in the middle ear. Inflammatory mediators important in OM are produced by infiltrating immune cells such as neutrophils, monocytes and lymphocytes. The middle ear tissues are able to produce inflammatory cytokines and use nuclear factor kappa B cell (NF-κB) activation.10 Complement, one of the first mediators activated in the initiation of inflammation throughout the body, is activated in OM also.11,12 It appears that complement itself may be harmful to the middle ear mucosa. Membrane cofactor protein (MCP) and protectin (CD59) are two middle ear proteins, which help prevent unrestricted complement damage.13

Cytokines Cytokines are glycoproteins, produced by inflammatory cells and epithelial cells, which modulate the immune response. The present theory is that cytokines are responsible for many of the inflammatory changes induced by pathogenic organisms during OM. Interleukin (IL-1) and tumor necrosis factor (TNF-α) are early response cytokines with IL-1 being a more potent activator than TNF-α.14 The IL-1 is comprised of two principal 17 kDa polypeptides: 1. IL-1α. 2. IL-1β. IL-lβ has been shown to play an important role in the pathogenesis of otitis media with effusion (OME). Barzilai et al.15 showed that IL-1 levels were significantly higher in culture-positive versus culture-negative AOM. Therefore, treatment that reduces IL-1β may be an effective adjuvant in the early stage of OM in children. The results of these studies suggest a potential therapeutic role with the clinical application of TNF inhibitors, such as TNF-binding protein or inhibitor TNF soluble receptor, to control the symptoms of AOM or to prevent chronicity and recurrence of OM.16,17

Mast Cells Mast cells are the most numerous resident leukocytes in the middle ear. When activated, mast cells release preformed mediators, histamine and tryptase, and also de novo synthesized mediators, leukotrienes and prostaglandins. Mast cells also release various cytokines including TNF and IL-1. Histamine is released by the mast cells present in the middle ear upon activation, by either complement or binding of antigen to immunoglobulin (IgE) antibodies, which study the exterior surface of mast cells. Through its vasodilatory effects, histamine can cause mucociliary and eustachian tube dysfunction.

Inflammatory Cells in Acute and Chronic Otitis Media Neutrophils are the predominant cells involved in early host response against OM during invasion of bacterial pathogens. Neutrophils have been shown to be associated with the pathogenesis of not only AOM but also chronic otitis media

58  Current Concepts of Otitis Media and Recent Management Strategies with effusion (COME) in children. In COM with repeated episodes of acute inflammation, neutrophils and macrophages infiltrate with each episode. As the inflammatory process enters a chronic phase, there is a continuing shift in the population of infiltrating leukocytes toward increasing numbers of mononuclear cells.

REFERENCES 1. Roland PS. Chronic suppurative otitis media: a clinical overview. Ear Nose Throat J. 2002;81(8 Suppl. 1):8-10. 2. Kenna MA, Bluestone CD, Reilly JS, et al. Medical management of chronic suppurative otitis media without cholesteatoma in children. Laryngoscope. 1986;96(2):146-51. 3. Vartiainen E. Results of surgical treatment for chronic noncholesteatomatous otitis media in the pediatric population. Int J Pediatr Otorhinolaryngol. 1992;24(3):209-16. 4. Lim DJ, Hussl B. Human middle ear epithelium. An ultrastructural and cytochemical study. Arch Otolaryngol. 1969;89(6):835-49. 5. Shimada T, Lim DJ. Distribution of ciliated cells in the human middle ear. Electron and light microscopic observations. Ann Otol Rhinol Laryngol. 1972;81(2):203-11. 6. Atef A, Ayad EE. Ciliary count in chronic suppurative otitis media: comparative quantitative study between mucosal and squamous types using scanning electron microscopy and image analysis. J Laryngol Otol. 2004;118(5):343-7. 7. Wright CG, Meyerhoff WL. Pathology of otitis media. Ann Otol Rhinol Laryngol Suppl. 1994;163:24-6. 8. Juhn SK, Jung MK, Hoffman MD, et al. The role of inflammatory mediators in the pathogenesis of otitis media and sequelae. Clin Exp Otorhinolaryngol. 2008;1(3): 117-38. 9. Juhn SK, Garvis WJ, Lees CJ, et al. Determining otitis media severity from middle ear fluid analysis. Ann Otol Rhinol Laryngol Suppl. 1994;163:43-5. 10. Ghaheri BA, Kempton JB, Pillers DA, et al. Cochlear cytokine gene expression in murine chronic otitis media. Otolaryngol Head Neck Surg. 2007;137(2):332-7. 11. Bernstein JM, Schenkein HA, Genco RJ, et al. Complement activity in middle ear effusions. Clin Exp Immunol. 1978;33(2):340-6. 12. Meri S, Lehtinen T, Palva T. Complement in chronic secretory otitis media. C3 breakdown and C3 splitting activity. Arch Otolaryngol.1984;110(12):774-8. 13. Narkio-Makela M, Jero J, Meri S. Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. Clin Exp Immunol. 1999;116(3):401-9. 14. Kunkel SL. Inflammatory cytokines. In: Ward PA, (Ed). Manual of vascular mediators. New York: HP Publishing Company; 1993. pp. 2-14. 15. Barzilai A, Leibovitz E, Laver JH, et al. Dynamics of interleukin-1 production in middle ear fluid during acute otitis media treated with antibiotics. Infection. 1999;27(3):173-6. 16. Ball SS, Prazma J, Dais CG, et al. Role of tumor necrosis factor and interleukin-1 in endotoxin-induced middle ear effusions. Ann Otol Rhinol Laryngol. 1997;106(8): 633-9. 17. Maxwell K, Leonard G, Kreutzer DL. Cytokine expression in otitis media with effusion. Tumor necrosis factor soluble receptor. Arch Otolaryngol Head Neck Surg. 1997;123(9):984-8. 18. Available from www.emedicine.medscape.com/article/859501.

11

Prevention of Acute Otitis Media L Paul Emerson, Anand Job

APPROACH TO THE CHILD WITH RECURRENT INFECTIONS Respiratory infections are common and frequent diseases and presents as one of the major complaints in children and adolescents. The role of physicians and other healthcare providers has expanded from merely treating disease to implementing measures aimed at health maintenance and disease prevention (Bellanti, 1997).1 Recurrent upper respiratory infections (URIs) are well known to cause acute otitis media (AOM). Also known is the fact that recurrent AOM is an important predisposing factor in the development of chronic otitis media (COM). Toward prevention of AOM and COM, it is necessary to diagnose and treat recurrent URIs (Flow chart 1). In this chapter, we aim to differentiate the child with primary immuno­ deficiency from the normal child who has more than the average number of viral infections and the child who has an underlying chronic disease that mimics infection, predisposing the child to certain types of infections, and results in secondary immune system dysfunction. These children can be differentiated by history, physical examination and certain screening investigations. This would

Flow chart 1  Various factors leading to otitis media

Abbreviations: LTs, leukotrienes; OME, otitis media with effusion; PAF, platelet-activating factor; PGs, prostaglandins

60  Current Concepts of Otitis Media and Recent Management Strategies ultimately determine the management plan including prevention strategies for these children.

PREDISPOSING FACTORS The increased prevalence of recurrent respiratory infection (RRI) in younger children could be attributed to the several factors2 such as, increased exposure to infectious agents during the initial years of life, especially at preschool or school, general immaturity of the immune system of younger children, social and environmental factors, e.g. large family size, overcrowding, air pollution, parental smoking,3 home dampness, climate, prematurity, low body weight infants, reduction of breastfeeding, positive family history of atopic diseases, pets at home (especially cats and dogs), poor socioeconomic conditions with malnutrition and missed vaccination.2 This is seen more often in the following circumstances: • A history of multiple episodes of AOM • Living in crowded conditions • Day care facility attendance • Being a member of a large family. Patients with craniofacial anomalies are special populations at risk. Cleft palate, Down syndrome, cri du chat syndrome, choanal atresia, cleft lip and microcephaly are other diagnoses that increase the risk of COM, from eustachian tube dysfunction.4,5 Also diseases such as chronic adenoiditis, chronic tonsillitis, chronic and allergic rhinosinusitis, chronic bronchitis can cause persistence, and recurrence of infection needs to be treated.

“NORMAL” CHILD Recurrent Infections Recurrent infections are defined as two or more severe infections in 1 year or three or more respiratory infections (e.g. sinusitis, otitis media and bronchitis) in 1 year, or the need for antibiotics for 2 months in a year.6

Severe/Serious Infections Severe/serious infections include those with persistent fever or confinement to bed for a week or more, failure to respond to oral antibiotics requiring intravenous antibiotics and needing hospitalization, infections with an unusual pathogen, unusual complications (e.g. mastoiditis, pleural effusion, abscesses), or persistent laboratory abnormalities [e.g. leukocytosis, elevated erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP) and persistent imaging abnormalities].7,8 About 50% of children with recurrent infections referred for evaluation, have no known significant cause for these infections. Infants and children vary considerably as to the number of infections experienced. The average child has four to eight respiratory infections/year. Some infants and young children who are kept away from strangers, have only one or two infections/year. Others may

Prevention of Acute Otitis Media 61 have 10–12 infections/year, particularly if they have older siblings or if they attend day care or preschool.9 The mean duration of viral respiratory symptoms is 8 days.10 However, the normal range can extend beyond 2 weeks, which means that the ‘normal’ child with over 10 viral respiratory infections, can have symptoms for nearly one-half of a year. With regard to the number and types of infections seen, most of the respiratory infections are viral.11 These children generally do not have more than one episode of pneumonia or more than two episodes of uncomplicated otitis media in the first 3 years of life. They have normal growth and development, respond quickly to appropriate treatment, recover completely, and appear healthy between infections. Physical examination and laboratory tests are normal.

CHILD WITH ATOPIC DISEASE About 30% of children with recurrent infections have atopic disease presenting as chronic allergic rhinitis and bronchitis, mistaken for chronic or recurrent URIs.12 Children with atopic disease often develop coughing and wheezing following viral respiratory infections. These symptoms are frequently misdiagnosed as pneumonia or bronchitis rather than reactive airways disease/asthma. These episodes respond poorly to antibiotics, but well to allergy/asthma medications. Children with atopic disease are more likely to develop recurrent and persistent URIs, such as sinusitis (Fig. 1), rhinitis and recurrent otitis media due to associated eustachian tube dysfunction.13 This increased susceptibility to infection may be due to the enhanced adherence of pathogens to inflamed

Fig. 1  Development of sinusitis in a person

62  Current Concepts of Otitis Media and Recent Management Strategies respiratory epithelium or alteration in mucosal permeability.14 Children with atopy, often have characteristic physical findings, such as ‘allergic shiners’ or a transverse nasal crease. It should be noted that primary immunodeficiency and allergies can coexist.

CHILD WITH CHRONIC DISEASE Ten percent of children with recurrent infections have an underlying chronic disease other than atopy or immunodeficiency.15 The child with a nonimmune chronic illness often presents with poor growth/failure to thrive, a sickly appearance and physical findings characteristic of the specific chronic disease. Diseases in this category include cystic fibrosis, gastroesophageal reflux, congenital heart disease and chronic aspiration. Patients can also have an underlying anatomic defect. Children present with recurrent nasal, sinus and throat infections. Some have tonsillar and adenoidal hypertrophy and secondary eustachian tube dysfunction. In such children, adenoidectomy and tonsillectomy are performed as per the validated guidelines.16 Those children with sinus infection, may need appropriate drainage procedures as well (Fig. 2). Continuous reinfection may be also due to contaminated water supply or chronically infected pet. Foreign body should be considered when the infection is localized to one anatomical site, such as one nostril.

CHILD WITH AN IMMUNODEFICIENCY Ten percent of children with recurrent infections have an immunodeficiency, with a defect in one or more components of the immune system.

Fig. 2  Pressure equalizing tube is required in case of recurrent ear infections

Prevention of Acute Otitis Media 63 A child with two or more sinus infections or pneumonias in 1 year, eight or more ear infections (otitis media) within 12 months, should be evaluated for immunodeficiency. In addition, children who have two or more invasive infections in the history (meningitis, cellulitis, osteomyelitis and septicemia), or failure of an infant to gain weight or grow normally, chronic diarrhea should be evaluated.17-19 If there is a positive history for immunodeficiency, a detailed immunological investigation is mandatory. In other children, immunological examination should be performed after excluding other, more frequent causes of RRI such, as gastroesophageal reflux, allergy or ear nose throat (ENT) focal infection e.g. adenoidal hypertrophy (Figs 3A to G).

Investigations for a Child Presenting to the Ear Nose Throat Specialist The following investigations are useful as a screening test in the diagnosis of RRI:20,21 • Blood count for eosinophilia • Nasal smear for eosinophil • Soft tissue X-ray of the nasopharynx or endoscopy, to look for adenoidal hypertrophy • Nasal endoscopy for sinusitis or X-ray of the paranasal sinuses • Specific immunoglobulin (IgE) levels • Skin prick test • Bacterial culture from nose/nasopharynx.

Figs 3A to G  Children with different health situations: (A) Normal child, not a problem; (B) Hardly a problem; (C) Somewhat a problem; (D) Moderate problem; (E) Quite a bit of a problem; (F) Very much a problem; (G) Extensive problem

64  Current Concepts of Otitis Media and Recent Management Strategies

Treatment and Prevention By evaluating the child using history, examination and investigations, the cause for RRI can be determined; to see whether these are of host-derived factors or the result of increased environmental exposure. Host-derived factors may be nonimmunological and immunological (related to host immunodeficiency). Accurate environmental prophylaxis and regimen changes are crucial for successful treatment, such as removal of environmental risk factors (e.g. precocious day care attendance, reducing the smoking in the household). Postponed enrollment of children at day care centers may be necessary for the prevention and decrease in the number of RRI. Optimal day care center enrollment with only a limited number of children, having large clean rooms with a good ventilation to guarantee the removal of the air suspended microbial agents and location in areas with less air pollution, are necessary measures.2 Breast milk contains a variety of substances with antimicrobial, antiinflammatory and immunomodulatory activity. Oligosaccharides in breast milk induce gut colonization with lactobacilli and bifidobacteria play an important role in the development of mucosal and systemic immune system. Breast milk is also rich in nucleotides with immunomodulatory activity and humoral response.22

Probiotics Probiotics are live microorganisms which when administered in adequate amounts, cause correct maturation of the immune system and reduce the development of allergy. The most common bacteria in this group are bifidobacteria and lactobacilli.23

Vitamins and Minerals Vitamins and minerals are needed for normal immune system function. Low levels are seen in malnourished children and can influence the frequency and duration of respiratory infections in them. Vitamin C seems to reduce the duration and severity of symptoms.24

MANAGEMENT OF ALLERGY Allergen Avoidance Dust Mite Although dust mites cannot be completely eliminated, it is possible to reduce significantly their numbers and exposure.

Allergen-proof Bed Covers The mattress and pillows are covered in dust-proof covers, which are made of tightly woven fabric, and prevent dust mites from colonizing.25,26 All the bed linen is washed in hot water that is at least 130°F (54.4°C), once a week to kill dust mites and to remove allergens. The bedding can be put out in the Sun. Washable stuffed toys should be washed as needed in hot water and dried and kept off the beds.

Prevention of Acute Otitis Media 65 A damp cloth is used to clean dust, which prevents it from becoming airborne and resettling. Vacuuming of carpets and upholstered furniture is preferred. Staying out of a dusted room for 20 minutes is helpful. Keeping the room tidy prevents accumulation of dust. Carpeting provides a comfortable habitat for dust mites, especially if it is over concrete, which holds moisture easily and provides a humid environment. Tile, wood, linoleum or vinyl flooring is better. Dust collects in upholstered furniture, nonwashable curtains and horizontal blinds, and should be addressed. Cat and dog dander can be controlled to some extent by bathing the pet once a week and regular grooming. Cockroaches need to be exterminated. Care should be taken to remove certain plants that are known to cause allergy, such as parthenium.27,28

Medications Used Oral Antihistamines Desloratadine and levocetirizine are nonsedating second generation antihistamines with fewer adverse effects than first generation. These compete with histamine for H1 receptors in the gastrointestinal (GI) tract, blood vessels and respiratory tract, reducing hypersensitivity reactions. Intranasal antihistamine sprays are also available.29 Montelukast is an antagonist to the leukotriene receptor. It is nonsedating, dosed once daily and has a safety profile similar in adults and children with approval down to 6 months of age. In the treatment of seasonal allergic rhinitis, its benefits are equivalent to antihistamines, when used as monotherapy, but less than intranasal corticosteroids.30 The addition of an antihistamine to montelukasts does appear to have added benefits and at times is reported to be equivalent to intranasal corticosteroids. Intranasal corticosteroids are potent anti-inflammatory agents shown to decrease allergic rhinitis symptoms in more than 90% of patients. Multiple medications are available and all are essentially equivalent in efficacy although mometasone and fluticasone furoate seem to have a faster onset of action; however, after 1 week, no difference is found. They can be used on a once-daily basis. Mometasone did not show an effect on growth. Saline nasal spray washes out the allergens from the nasal cavity and is effective in 50% of patients. Nasal decongestants such as xylometazoline and oxymetazoline provide immediate relief of nasal congestion. However, their effect is temporary and rhinitis medicamentosa is a well known side effect, if used regularly. Ipratropium nasal spray 0.03% is helpful in those who face profuse rhinorrhea. Chemically related to atropine, this has antisecretory properties and when applied locally, inhibits secretions from the serous and seromucous glands. It is poorly absorbed by nasal mucosa and therefore not associated with adverse systemic effects. Local adverse effects such as dryness, epistaxis and irritation may occur.31

Indication for Antibiotics Although viruses are the predominant cause of respiratory infections, bacterial pathogens, commonly Streptococus pneumoniae, Haemophillus influenzae,

66  Current Concepts of Otitis Media and Recent Management Strategies Mycoplasma pneumoniae, Chlamydophila pneumoniae and Moraxella catarr­ halis have been isolated32 and in the acute phase, require to be used. Recurrent viral infections are part of the growing up process of any child; hence giving antibiotics at every episode to cover ‘so-called superadded bacterial infections’ will lead to resistance. Prophylactic antibiotics are neither indicated nor useful and even could interfere with normal development of the mucosal microflora and immune system functions. Instead, efforts should be made to treat the underlying cause. Antibiotics are used in the acute phase, only when bacterial pathogens are suspected depending on the severity of infection and administered in adequate dose and duration. Adequate drainage of the sinuses, tonsillectomy and adenoidectomy form important adjuvant therapies. White blood cell (WBC) count can aid judicious antibiotic prescribing in acute URIs.33 In patients with significant respiratory or febrile illness, a WBC count greater than 15,000/mms, benefit from antibiotics. With this approach, no child who had significant bacterial illness will be missed. Children at highest risk for developing resistant bacteria are those who have failed previous treatments, have had numerous previous antibiotic prescriptions, or received low doses of antibiotics over a prolonged period. Hence, opinion is divided over the use of antibiotic prophylaxis. Preventive antibiotics are usually given to children who have at least three episodes of respiratory tract infections (RTIs) within a 6 month period. Physician’s opinion varies as to the best timing for these antibiotics. They may be given for a consistent 3–6 month period, following the last acute episode. Some physicians may prescribe them only in winter and spring, when the risk for respiratory infections is high. The preventive regimen is one or two daily doses of amoxicillin or sulfisoxazole. Simple measures for prevention of colds such as eating adequate fruits and vegetables, getting enough rest, and washing hands frequently, need to be reemphasised. New antibacterial soaps add little protection and ordinary soaps are sufficient. In fact, a recent study suggests that common liquid dishwashing soaps are up to 100 times more effective than antibacterial soaps in killing respiratory syncytial virus (RSV), which is known to cause pneumonia.

REFERENCES 1. Bellanti JA. Recurrent respiratory tract infections in paediatric patients. Drugs. 1997;54 Suppl 1:1-4. 2. de Martino M, Balloti S. The child with recurrent respiratory infections: normal or not? Pediatr Allergy Immunol. 2007;18 Suppl 18:13-8. 3. Environmental tobacco smoke: a hazard to children. American Academy of Pediatrics Committee on Environmental Health. Pediatrics. 1997;99(4):639-42. 4. Boston M, McCook J, Burke B, et al. Incidence of and risk factors for additional tympanostomy tube insertion in children. Arch Otolaryngol Head Neck Surg. 2003;129(3):293-6. 5. Balkany TJ, Downs MP, Jafek BW, et al. Otologic manifestations of Down’s syndrome. Surg Forum. 1978;29:582-5. 6. ER Stiehm. Approach to the child with recurrent infections. UpToDate website. Available from http://www.uptodate.com/contents/approach-to-the-child-withrecurrent-infections [Accessed November, 2013].

Prevention of Acute Otitis Media 67 7. Campbell H. Acute respiratory infection: a global challenge. Arch Dis Child. 1995;73(4):281-3. 8. Grüber C, Keil T, Kulig M, et al. History of respiratory infections in the first 12 yr among children from a birth cohort. Pediatr Allergy Immunol. 2008;19(6):505-12. 9. Monto AS. Viral respiratory infections in the community: epidemiology, agents, and interventions. Am J Med. 1995;99(6B):24S-27S. 10. Bush A. Recurrent respiratory infections. Pediatr Clin North Am. 2009;56(1):67-100. 11. Treanor JJ, Hayden FG. Viral infections. In: Murray JF, Nadel JA, Mason R, Boushey HA (Eds). Textbook of Respiratory Medicine, 3rd edition. Philadelphia, PA: WB Saunders; 2000. 12. Dellepiane RM, Pavesi P, Patria MF, et al. Atopy in preschool Italian children with recurrent respiratory infections. Pediatr Med Chir. 2009;31(4):161-4. 13. Ghezzi M, Silvestri M, Guida E, et al. Acid and weakly acid gastroesophageal refluxes and type of respiratory symptoms in children. Respir Med. 2011;105(7):972-8. 14. Ballow M. Approach to the patient with recurrent infections. Clin Rev Allergy Immunol. 2008;34(2):129-40. 15. Bonilla FA, Bernstein IL, Khan DA, et al. Practice parameter for the diagnosis and management of primary immunodeficiency. Ann Allergy Asthma Immunol. 2005;94(5 Suppl 1):S1-63. 16. Frohna JG. Effectiveness of adenotonsillectomy in children with mild symptoms of throat infections of adenotonsillar hypertrophy: open, randomized controlled trial. J Pediatr. 2005;146(3):435-6. 17. Stiehm ER, Ochs HD, Winkelstein JA. Immunodeficiency disorders: general considerations. In: Stiehm ER, Ochs HD, Winkelstein JA (Eds). Immunologic disorders in infants and children, 5th edition. Philadelphia, PA: Saunders/Elsevier; 2004. p.289. 18. Wheeler JG. Evaluating the child with recurrent infections. Am Fam Physician. 1996;54(7):2276-820. 19. Carneiro-Sampaio M, Jacob CM, Leone CR. A proposal of warning signs for primary immunodeficiencies in the first year of life. Pediatr Allergy Immunol. 2011;22(3):345-6. 20. de Vries E. Immunological investigations in children with recurrent respiratory infections. Paediatr Respir Rev. 2001;2(1):32-6. 21. Slatter MA, Gennery AR. Clinical immunology review series: an approach to the patient with recurrent infections in childhood. Clin Exp Immunol. 2008;152(3):389-96. 22. Jones KD, Berkley JA, Warner JO. Perinatal nutrition and immunity to infection. Pediatr Allergy Immunol. 2010;21(4 Pt 1):564-76. 23. Galdeano CM, Perdigón G. The probiotic bacterium Lactobacillus casei induces activation of the gut mucosal immune system through innate immunity. Clin Vaccine Immunol. 2006;13(2):219-26. 24. Douglas RM, Hemila H, D’Souza R, et al. Vitamin C for preventing and treating the common cold. Cochrane Database Syst Rev. 2004;(4):CD000980. 25. Wan H, Winton HL, Soeller C, et al. Der p 1 facilitates transepithelial allergen delivery by disruption of tight junctions. J Clin Invest. 1999;104(1):123-33. 26. Ghaemmaghami AM, Robins A, Gough L, et al. Human T cell subset commitment determined by the intrinsic property of antigen: the proteolytic activity of the major mite allergen Der p 1 conditions T cells to produce more IL-4 and less IFN-gamma. Eur J Immunol. 2001;31(4):1211-6. 27. Miller JD, Miller A. Ten minutes in a clothes dryer kills all mites in blankets. J Allergy Clin Immunol. 1996;97:423. 28. McDonald LG, Tovey E. The role of water temperature and laundry procedures in reducing house dust mite populations and allergen content of bedding. J Allergy Clin Immunol. 1992;90(4 Pt 1):599-608.

68  Current Concepts of Otitis Media and Recent Management Strategies 29. Gentile DA, Friday GA Jr, Skoner DP. Management of allergic rhinitis: Antihista­ mines and decongestants. Immunol Allergy Clin North Am. 2000;20:355. 30. Chervinsky P, Philip G, Malice MP, et al. Montelukast for treating fall allergic rhinitis: effect of pollen exposure in 3 studies. Ann Allergy Asthma Immunol. 2004;92(3):36773. 31. Milgrom H, Biondi R, Georgitis JW, et al. Comparison of ipratropium bromide 0.03% with beclomethasone dipropionate in the treatment of perennial rhinitis in children. Ann Allergy Asthma Immunol. 1999;83(2):105-11. 32. Garenne M, Ronsmans C, Campbell H. The magnitude of mortality from acute respiratory infections in children under 5 years in developing countries. World Health Stat Q. 1992;45(2-3):180-91. 33. Casey JR, Marsocci SM, Murphy ML, et al. White blood cell count can aid judicious antibiotic prescribing in acute upper respiratory infections in children, Clin Pediatr (Phila). 2003;42(2):113-9.

12

Vaccination for Preventing Acute Otitis Media L Paul Emerson, Anand Job

PREVENTION OF RECURRENT ACUTE OTITIS MEDIA The value of preventing recurrent acute otitis media (AOM) is that it can potentially decrease acute febrile illnesses in children and prevent chronic otitis media. Prevention can be achieved by decreasing nasopharyngeal colonization by the three important pathogens that cause AOM, establishing correct feeding methods, improve socioeconomic status and decreased air pollution.

Clinical Impact of Vaccinations on Acute Otitis Media Acute otitis media is common in infants and children experience atleast one episode in the 1st year of life and up to 50% suffer from recurrent episodes.1,2 Although approximately two third of cases are due to bacteria, almost all the episodes are preceded by upper respiratory viral infections. Also as evidence, respiratory syncytial virus and influenza virus have been isolated from the middle ears. It has been demonstrated that the influenza virus alters the respiratory mucosa in a way that it predisposes to adherence, invasion and induction of disease by Pneumococcus. Vaccine prevention of influenza can be used as a means of reducing the risk of AOM, particularly in otitis-prone children and also to reduce their predisposition to pneumococcal infection. This benefit is enhanced when the individual episodes of AOM are not complicated by perforation of the tympanic membrane.

Pneumococcal Vaccination Pneumococcal conjugate vaccine (PCV7) is highly immunogenic in children in the first few months of life and includes most of the serotypes associated with AOM (4, 6B, 9V, 14, 19F, 18C and 23F). As Streptococcus pneumoniae is the cause of 25–50% of the cases of AOM and PCV7 prevented more than 90% of the cases of invasive pneumococcal disease (IPD), it was thought that a significant reduction in the incidence of AOM might follow the implementation of programs for its universal use in younger children. It was reported that after the introduction of PCV7, the rates of otorrhea visits/10,000 emergency department visits, decreased by 38% (p < 0.001), mainly as a result of the decrease in the incidence of pneumococcal disease. It has been suggested that there could be an indirect effect, such as unvaccinated and partially vaccinated children possibly being protected and as a result of the reduced carriage and the transmission of vaccine serotypes by vaccinated children.

70  Current Concepts of Otitis Media and Recent Management Strategies The serotypes added to PCV10 are 1, 5 and 7F, and eight of the ten serotypes are conjugated to a recombinant nonlipidated form of protein D, a 42 kDa cell surface lipoprotein of Hemophilus influenzae that acts as a carrier protein for pneumococcal antigens and simultaneously elicits a significant immune response against H. influenzae. It was therefore, thought that this PCV would not only extend protection against pneumococcal AOM, but also induce protection against AOM due to nontypeable H. influenzae, the second most important bacterial cause of this disease. The efficacy of these vaccines have been made on the basis of the change in nasopharyngeal colonization induced by PCV7, the risk of AOM in colonized children and the potential impact on carriage. In 2010, a PCV, which protects against an additional six serotypes was introduced (PCV13). It has been calculated that the total number of AOM cases caused by PCV13 should decline from 53% in 2007 to 19% in 2013 and that the global reduction in pneumococcal AOM could reach 2.7% and that of all-cause AOM could reach more than 10%. An exact evaluation of the role of influenza vaccination in preventing AOM was hampered by factors including the enrollment of children at different degrees of risk for AOM, the use of the reduction in all-cause AOM instead in influenza-associated AOM as reference for efficacy testing the administration of vaccines with various degrees of immunogenicity against influenza viruses. In a meta-analysis of randomized studies, the efficacy of influenza vaccination against AOM (of any cause) in healthy children younger than 18 years was 51% (95% confidence interval 21–70%).3

VACCINE SCHEDULE Routine Schedule The routine pneumococcal vaccine schedule for healthy and high-risk children in the United States is as follows: • Healthy children less than 24 months should receive a total of four doses of the 13-valent PCV13 at 2, 4, 6 months, and 12–15 months of age.4 The first dose can be given as early as 6 weeks of age. A minimum of 4 weeks between the three doses is acceptable in children younger than 1 year. The fourth dose should be given at 12–15 months of age, but at least 8 weeks after the third dose. Preterm infants should receive PCV13 according to their chronologic age5. • Children at high risk of invasive pneumococcal disease (IPD) who are younger than 24 months should receive PCV13 according to the schedule for healthy children. In addition, high-risk children more than 2 years of age should receive the 23-valent pneumococcal polysaccharide vaccine (PPSV23) at least 8 weeks after they have completed immunization with PCV13. • High-risk children younger than 72 months, who completed immunization with the 7-valent PCV7 and PPSV23 should receive a single dose of PCV13 at least 8 weeks after the last dose of PCV7 or PPSV23. The polysaccharide 23-valent vaccine is poorly immunogenic in young children. Immunization is suggested for those at highest risk of infection, including those 65 years or older. The current guidelines of the American

Vaccination for Preventing Acute Otitis Media 71 College of Physicians, calls for the administration of immunization between ages 2 years and 65 years when indicated or at age 65 years. If someone received the immunization before age 60 years, the guidelines call for a one-time revaccination. Revaccination at periodic intervals is also indicated for those with other conditions such as asplenia or nephrotic syndrome.

REFERENCES 1. Armengol CE, Hendley JO, Winther B. Occurrence of acute otitis media during colds in children younger than four years. Pediatr Infect Dis J. 2011;30(6):518-20. 2. Morris PS, Leach AJ. Acute and chronic otitis media. Pediatr Clin North Am. 2009;56(6):1383-99. 3. Manzoli L, Schioppa F, Boccia A, et al. The efficacy of influenza vaccine for healthy children: a meta-analysis evaluating potential sources of variation in efficacy estimates including study quality. Pediatr Infect Dis J. 2007;26(2):97-106. 4. Nuorti JP, Whitney CG. Centers for disease control and prevention (CDC). Prevention of pneumococcal disease among infants and children—use of 13-valent pneumococcal conjugate vaccine and 23-valent pneumococcal polysaccharide vaccine—recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2010;59(RR-11):1-18. 5. D’Angio CT, Heyne RJ, O’Shea TM, et al. Heptavalent pneumococcal conjugate vaccine immunogenicity in very-low-birth-weight, premature infants. Pediatr Infect Dis J. 2010;29(7):600-6.

13

Eosinophilic Otitis Media L Paul Emerson, Anand Job

INTRODUCTION Eosinophilic otitis media (EOM) is an important entity to be considered in the differential diagnosis and management of chronic otitis media (COM).1 This disease is suspected when the ear fails to become dry with conventional treatment or when tympanoplasty fails with recurrence of discharge, or when the patient develops progressive or sudden sensorineural hearing loss (SNHL) during the course of the disease or following tympanoplasty. This condition was first reported by Koch in cases of patients with middle ear effusion (MEE), which contained many eosinophils.2 The term EOM was coined by Tomioka et al in 1993.3 This intractable condition is characterized by the presence of viscous yellow MEE leading to perforation of the pars tensa of the tympanic membrane with persistent ear discharge and polyp formation.

CLINICAL FEATURES Eosinophilic otitis media predominantly affects women and presents most often in patients in their 50s. The clinical presentation is divided into: • Those who develop otitis media with effusion and • Those presenting with COM. The latter is further divided into two subtypes: 1. Simple perforation and 2. Those presenting with granulation tissue also. High-tone SNHL is more frequently found and more severe in EOM patients than in COM control patients.4 Eosinophilic otitis media is often complicated by rhinosinusitis (eosinophilic sinusitis).

Criteria for Clinical Diagnosis • Major – Otitis media with effusion or COM with eosinophil dominant effusion. • Minor – Highly viscous MEE – Otitis media resistant to conventional treatment – Association with bronchial asthma – Association with nasal polyposis.

Eosinophilic Otitis Media 73

Definitive Case Major and two or more minor criteria.

Exclusion Criteria Churg-Strauss syndrome and hypereosinophilic syndrome.

Pathogenesis Lino et al. suggested that in patients with T helper type 2 dominant predisposition, such as in bronchial asthma, antigenic material traverses the eustachian tube and stimulates middle ear inflammation, resulting in accumulation of eosinophils, which further induces fibroblasts or endothelial cells to produce eosinophil chemoattractants.2 The cytotoxic proteins and active oxygen species generated by eosinophils may damage the epithelial layer, including the round window membrane and lipid mediators released from eosinophils render the membrane permeable. These events allow inflammatory substances such as bacterial toxins and inflammatory cytokines to enter into the middle and inner ear, causing hair cell damage and SNHL. Systemic or topical glucocorticoid (triamcinolone) is most effective in countering this process. The presence of a highly viscous effusion containing eosinophils and high levels of immunoglobulin (IgE) in the MEE is characteristic of this disease. Also, high blood levels of IgE have been detected. Biopsy of the middle ear mucous membrane shows eosinophilic infiltration, goblet cell metaplasia; chronic inflammatory granulation tissue and fibril formation in the epithelial and subepithelial tissue in the advanced stages similar to asthma.5 Charcot-Leyden crystals are also seen.

Clinical Findings Eosinophilic otitis media is characterized by extremely viscous mucoid effusion and may be associated with a history of adult bronchial asthma, nasal allergy or nasal polyposis. It usually causes unilateral/bilateral otitis media, resistant to the conventional treatment for otitis media with effusion (OME) or COM. It may present as a bulging yellowish ear drum without perforation along with deteriorating hearing. Patients also present with persistent ear discharge with a pars tensa perforation and granulations arising from the mesotympanum leading to polyp formation. In some patients, the eustachian tube was found to be patulous. High frequency SNHL or mixed hearing loss, which can be progressive and occasional sudden sensorineural loss are known to occur.

Investigations On computed tomography (CT) scan imaging, findings of EOM might be similar to COM, with heterogeneous soft tissue within the middle ear predominantly mesotympanum and mastoid, with or without erosion of the ossicles. Inflammatory changes are seen in the eustachian tube as well. Some features more in favor for EOM than COM on CT and magnetic resonance imaging (MRI)

74  Current Concepts of Otitis Media and Recent Management Strategies .

are a higher incidence of bilaterality with chronic rhinosinusitis and sinonasal polyposis.6 The differential diagnosis of cholesteatoma, keratosis obturans or medial canal fibrosis can be differentiated from EOM by the presence of bony erosion or predominant involvement of external auditory canal.

Management In patients presenting with OME, Toshiro et al7 proposed conservative treatment by injecting steroid solution into middle ear for resolution of disease and preservation of hearing. Also, grommet insertion has been suggested. It has been noted in patients with severe chronic recurrent otitis media with pars tensa perforation, tympanoplasty or mastoidectomy can make the disease worse. Although the exact mechanism has not known, Tomioka et al reported a patient who finally became deaf in both ears several years after ear surgery. A multi-institutional study showed a significantly higher ratio of SNHL among these patients, who underwent ear surgery as compared to those without tympanoplasty (17% vs 4%, p < 0.05). Iwasaki et al8 reported a patient with EOM postsurgery, who had developed a sudden onset of bilateral deafness and vertigo. On CT scan of the temporal bone, ossification of the cochlea on the symptomatic side was detected. The speculation was that the accumulated activated eosinophils induced by mastoid surgery may have increased the susceptibility of the infiltration of proteins into the inner ear, facilitated by tissue damage to the round window membrane. Recurrent ear infections, which fail to respond to conventional medical treatment, EOM should be considered and look for eosinophils in the middle ear discharge and also in the biopsy from the middle ear mucosa. Treatment is directed to keep the ear dry by using systemic or local steroids in the active stage and also in managing allergic sinusitis and bronchial asthma, which are known to coexist. Steroid administration is currently the most effective treatment for patients with EOM. The instillation of triamcinolone acetonide, into the middle ear is very effective for controlling eosinophilic inflammation.4 A pilot study showed recent evidence that long-term anti-IgE therapy (omalizumab) improved the clinical ear symptoms of EOM and bone conduction hearing levels were mostly preserved.9 Long-term anti-IgE therapy may be effective for EOM to inhibit eosinophilic inflammation in the middle ear. In the past, when the disease was unrecognized, it is possible that such patients underwent unsuccessful tympanoplasty and ultimately underwent canal wall down procedures for intractable ear discharge with SNHL. Surgery should not be considered, unless the ear has become completely inactive. Prior to surgery, it may be preferable to obtain a temporal bone CT scan to detect the extent of disease/granulation tissue and to rule out involvement of the mastoid, so that the surgery may be modified and cortical mastoidectomy may need to be considered without tympanoplasty until the ear is disease free. After surgery, medical management with systemic steroids may be needed to control the inflammation. It is important to counsel patients on the protracted course of disease. Disabling SNHL can be addressed with a hearing aid or cochlear implant.

Eosinophilic Otitis Media 75

CONCLUSION Eosinophilic otitis media (EOM) is an important entity is suspected when the ear fails to become dry with conventional treatment, or when tympanoplasty fails. Surgery should not be considered, unless the ear has become completely inactive. After surgery, medical management with systemic steroids may be needed to control the inflammation. SNHL can be addressed with a hearing aid or cochlear implant.

REFERENCES 1. Iino Y, Kakizaki K, Katano H, et al. Eosinophil chemoattractant in middle ear patients with eosinophilic otitis media. Clin Exp Allergy. 2005;35(10):1370-6. 2. Koch H. Allergical investigations of chronic otitis. Acta Otolaryngol. 1947;62:1-201. 3. Tomioka S, Yuasa R, Iino Y. Intractable otitis media in cases with bronchial asthma. Recent advances in otitis media. In: Mogi G, Honjo I, Ishii T, (Eds). Proceedings of the second extraordinary international symposium on recent advances in otitis media. amsterdam, New York: Kugler Publications; 1993. pp. 183-6. 4. Iino Y. Eosinophilic otitis media: A new middle ear disease entity. Curr Allergy Asthma Rep. 2008;8(6):525-30. 5. Okude A, Tagaya E, Kondo M, et al. A case of severe asthma with eosinophilic otitis media successfully treated with anti-ige monoclonal antibody omalizumab. Case Rep Pulmonol. 2012;2012:340-525. 6. Chung WJ, Lee JH, Lim HK, et al. Eosinophilic otitis media: CT and MRI findings and literature review. Korean J Radiol. 2012;13(3):363-7. 7. Kawano T, Ishitoya J, Endo R, et al. Conservative treatment of eosinophilic otitis media. Practica Oto-Rhino-Laryngologica. 2007;100(12):965-71. 8. Iwasaki S, Nagura M, Mizuta K. Cochlear implantation in a patient with eosinophilic otitis media. Eur Arch Otorhinolaryngol. 2006;263(4):365-9. 9. Iino Y, Hara M, Hasegawa M, et al. Clinical efficacy of anti-IgE therapy for eosinophilic otitis media. Otol Neurotol. 2012;33(7):1218-24.

14

Preoperative and Intraoperative Considerations Anand Job, L Paul Emerson, John Mathew

FACTORS THAT AFFECT SURGICAL DECISIONS There are many factors that have a bearing on the potential success of tympanoplasty. The presence of concomitant ossicular discontinuity and loss of ossicles with tympanic membrane perforation or adhesive otitis, eustachian tube dysfunction elevates the degree of difficulty and a tympanostomy tube may be required additionally. Tympanosclerosis has a significant adverse effect on the long term hearing outcome. The technical skills of the surgeon have a major effect as well as the type of graft material used as well as prosthesis selected. Inadequate exposure increases the degree of difficulty of the procedure. A vital decision to be made during surgery for chronic otitis media especially, in the presence of cholesteatoma is whether to perform ossiculoplasty at the same time or as a planned procedure some months later. Important factors relevant during surgery are: • Status of the middle ear mucosa • Amount of bleeding during surgery • Advisability of reoperation for possible cholesteatoma recurrence • Eustachian tubes function in the involved and the contralateral ear. If the middle ear mucosa is thickened, infected or granular and areas of unhealthy mucosa removed, it is likely to heal with fibrous tissue formation, which can displace a perfectly placed prosthesis over time. Middle ear bleeding obscures visualization and makes the surgery more difficult and increases the risk of unfavorable fibrosis. Some surgeons opt to perform ossiculoplasty in the same setting, even when there are areas of denuded mucosa, which need to heal and even when ‘second look’ procedure for recurrent or residual cholesteatoma is needed, due to economic considerations. Other surgeons stage the ossiculoplasty and at the initial surgery aim to eradicate the disease and decrease postoperative middle ear fibrous tissue by placing a sheet of silastic between the promontory and the tympanic membrane (graft). After healing is complete, the level of the tympanic membrane vis-à-vis the promontory is established and will be stable for the second-stage ossiculoplasty. This will make it easier to judge the appropriate length for a prosthesis that connects the tympanic membrane or malleus to the stapes capitulum or footplate. When the middle ear space is reduced (e.g. by chronic ear disease or canal wall down surgery), the impedance and pressure of the middle ear increase relative to the external canal, because the impedance of the middle ear space varies inversely with its volume. This reduction in pressure difference leads to a subsequent reduction in tympanic membrane and ossicular motion.

Preoperative and Intraoperative Considerations 77 The minimal amount of air required to maintain ossicular coupling within 10 dB of normal has been estimated to be 0.5 mL.1 Despite the fact that tubal function assessment is very difficult, an attempt is made to improve eustachian tube function in the preoperative and postoperative period. The patient was instructed to perform auto insufflation three times daily after surgery and if unable to insufflate the ear by 3 months, the ear was intubated. Using this protocol, it was found that the mucosal thickening is at least in part reversible and good results obtained.

Preoperative Considerations Resulting in Poor Outcomes Acute infection of the ear is an absolute contraindication for surgery, as it will most likely result in poor healing, prosthesis extrusion or both. Relative contraindications include persistent middle ear mucosal disease and repeated unsuccessful use of the same or similar prostheses. Although results are better in dry ears and in ears with healthy middle ear mucosa than in patients with active otorrhea, polypoidal granular middle ear disease and adhesive otitis, tympanosclerosis had the worst prognostic significance. Tympanosclerosis impaired the mobility of the ossicles and the cause of poor hearing is more due to refixation of the stapes, rather than the failure of reconstruction between the stapes head and the malleus handle.

Middle Ear Risk Index2,3 The term middle ear risk index (MERI) is used to predict the success rate of middle ear reconstructive procedures. Accurate prediction of the surgical results of ossiculoplasty depends on the status of the middle ear and its ossicles. AustinKartush initially classified a method to define the prereconstruction ossicular status. Four different groups have been identified: 1. Group A: Malleus and stapes present (commonly seen status) because of precarious vascularity of incus. 2. Group B: Malleus and foot plate of stapes present. 3. Group C: Malleus absent and stapes present. 4. Group D: Malleus and stapes suprastructure absent. Kartush further added three more classes as a modification to account for ossicular fixity: 1. O: Intact ossicular chain. 2. E: Ossicular head fixation. 3. F: Stapes fixation (Figs 1A to E). Middle ear risk index includes: • Austin-Kartush classification of ossicular defects as mentioned earlier • Bellucci4 classification: Bellucci classification gives weightage to otorrhea and is used as an index (Table 1). Perforation adds a value of one to the risk index: • Cholesteatoma, if present adds a value of two to the risk index • Presence of effusion/granulation in the middle ear adds two to the risk index • History of previous surgery adds two to the risk factor • History of smoking adds another two to the risk factor. Totaling all these factors we arrive at the middle ear risk index.

78  Current Concepts of Otitis Media and Recent Management Strategies

A

B

C

D

E

Figs 1A to E Austin-Kartush ossicular classification: (A) Class 0—Normal ossicles (M–Malleus, I–Incus, S–Stapes); (B) Class A: Absent incus (M–Malleus, S–Stapes); (C) Class B: Absent incus and stapes (M–Malleus, S–Stapes); (D) Class C: Absent malleus and incus (M–Malleus, S–Stapes); (E) Class A: Absent ossicles (M–Malleus, S–Stapes)

Preoperative and Intraoperative Considerations 79 Table 1  Bellucci classification Otorrhea

• • • •

Risk value

Dry ear

0

Occasionally wet

1

Persistently wet

2

Persistently wet with cleft palate

3

Risk categories can be derived from the MERI as follows: MERI 0–Normal MERI 1–3: Mild disease MERI 4–6: Moderate disease MERI 7–12: Severe disease.

Defining Success Attempts have been made to standardize reporting 1995 guidelines of the American Academy of Otolaryngology-Committee on Hearing and Equilibrium (AAO-CHE). Pre- and post-operative air conduction and bone conduction thresholds are measured at four designated frequencies (0.5, 1, 2 and 3 kHz) and averaged. Success is defined as a mean postoperative air bone gap of less than 20 dB and is the main outcome considered. It is clear that optimal results depend not only on the qualities of the prosthesis, but also on the environment in, which it is placed and the surgical techniques used. As a further development, Dornhoffer and Gardner proposed the ossicular outcomes parameters staging (OOPS) index. In their analysis, congenital cases and those patients with stapes fixation were excluded as they had unique problems and hence, the results different. Excluding these patients, for performing the ossiculoplasty, the Dornhoffer Hapex total ossicular replacement prosthesis (TORP) and partial ossicular replacement prosthesis (PORP) was used with standard lengths of 2 mm and 4 mm for PORP and TORP respectively. On analysis, they found that even in the presence of cholesteatoma, the overall results depended on the status of the middle ear mucosa. Hence, based on their findings, they have proposed a new classification for prognostic factors in ossiculoplasty (Table 2).5 The presence of malleus manubrium was found to be significant, whereas the stapes superstructure contributed little or nothing to the acoustic gain of the middle ear mechanism. The malleus may be significant acoustically through its action as a catenary lever and an impedance matcher, although the difference was only 2.9 dB in total ossiculoplasties. Canal wall down mastoidectomy and revision surgery also generated poorer hearing results. The percentage of patients closing their air-bone gap (ABG) to within 10 dB was 44% with 66% closing their ABG to within 20 dB. The mean four-frequency hearing gain was 15.7dB. The mean postoperative ABG was 15.7 dB. Prosthesis extrusion has been one of the reasons for failure of tympanoplasty and varied from 5% to 39% in the literature. The rate of extrusion depends on several factors, the most important of, which is the status of the middle ear and

80  Current Concepts of Otitis Media and Recent Management Strategies Table 2  Ossiculoplasty outcome parameters staging index Risk factor

Risk value

Middle ear factors Drainage  None

0

  Present > 50% of time

1

Mucosa  Normal

0

 Fibrotic

2

Ossicles  Normal

0

  Malleus +

1

  Malleus –

2

Surgical factors Type of surgery   No mastoidectomy

0

  Canal wall-up mastoidectomy

1

  Canal wall-down mastoidectomy

2

Revision surgery  No

0

 Yes

2

eustachian tube, the implant material, use of cartilage as tympanic membrane and the technique used. The following situations generally have a favorable prognosis for improved hearing: • Presence of malleus handle • Intact stapes arch • Mastoidectomy not required • First time surgery. Worst results typically occur in patients with congenital ossicular abnormalities.

REFERENCES 1. Merchant SN, Rosowski JJ, Ravicz ME. Middle ear mechanics of type IV and type V tympanoplasty: II. Clinical analysis and surgical implications. Am J Otol. 1995;16(5):565-75. 2. Kartush JM. Ossicular chain reconstruction. Capitulum to malleus. Otolaryngol Clin North Am. 1994;27(4):689-715. 3. Austin DF. Ossicular reconstruction. Arch Otolaryngol. 1971;94(6):525-35. 4. Bellucci RJ. Dual classification of tympanoplasty. Laryngoscope. 1973;83(11):1754-8. 5. De Vos C, Gersdorff M, Gérard JM. Prognostic factors in ossiculoplasty. Otol Neurotol. 2007;28(1):61-7.

15

Classification of Tympanoplasty Anand Job, L Paul Emerson, John Mathew

INTRODUCTION Tympanoplasty is a surgical procedure to eradicate middle ear disease and reconstruct the middle ear conducting mechanism with repair of the tympanic membrane (TM). The procedure may be staged depending on the middle ear condition and the ossicular status. The decision to perform either transcanal or endaural or retroauricular approach is ideally guided by the preoperative evaluation and has been dealt with in earlier sections (Flow chart 1).

Flow chart 1  Classification of tympanoplasty

82  Current Concepts of Otitis Media and Recent Management Strategies

CLASSIFICATION OF TYMPANOPLASTY Wullstein’s classification1 (modified by Job A, Emerson P and Mathew J): Wullstein’s classification takes into account the status of the TM and ossicles, as well as the method of reconstruction used. This classification continues to be widely used, as the outcome of various surgical techniques as well as graft materials can be compared. However, the status of the middle ear mucosa and eustachian tube function is excluded.

Type I Tympanoplasty Type I tympanoplasty is performed when all three ossicles are normal and mobile with perforation or retraction of the TM. Any disease is removed from the middle ear cleft and the TM perforation is repaired with temporalis fascia or with cartilage, if there is retraction of the TM remnant.

Type II Tympanoplasty Type II tympanoplasty is performed for minor ossicular defects. Usually, part of an ossicle or one of the ossicles is affected. It is divided into three subgroups: 1. Subtype 1: The malleus is defective; usually the handle is necrosed and needs using cartilage by underlay technique. 2. Subtype 2: The incus is necrosed and is divided into two groups: a) Minor ossicular loss: Usually the incus lenticular process or part of the long process is eroded and involves bridging the gap using a suitable prosthesis like an angular prosthesis. b) Major ossicular loss: Much of the long process or the entire incus is absent. The remnant is dislocated, refashioning and interposed or if absent, a bone or cartilage or partial ossicular replacement prosthesis (PORP) is placed between the malleus (usually handle or sometimes neck, if handle retracted) and stapes to restore the lever mechanism and the TM is reconstructed. 3. Subtype 3: Here, the stapes superstructure is eroded, which may include part of the long process of incus and reconstruction involves using the incus or bridging the gap with a PORP.

Type III Tympanoplasty Type III tympanoplasty is indicated when both incus and malleus are eroded (lateral ossicular erosion) and the stapes alone is intact and mobile. It is divided into two groups: 1. Classical type III tympanoplasty (following canal wall down mastoidectomy): The TM or graft is placed in contact with the stapes superstructure (myringostapediopexy or stapes columella), producing a shallow middle ear. This procedure is rarely done, when one has to do a canal wall down mastoidectomy. 2. Intact canal wall/reconstructed canal wall type III tympanoplasty: Minor columella reconstruction (cartilage, bone or PORP) from the stapes head to the TM is done. Cartilage interposition is needed between TM graft and PORP to prevent extrusion.

Classification of Tympanoplasty 83

Type IV Tympanoplasty Type IV tympanoplasty is done when a mobile stapes footplate is present and the handle of malleus may or may not be present. • Canal wall down and no columella: The footplate is left exposed with graft covering the round window niche and eustachian tube. The resulting middle ear (cavum minor) consists of hypotympanum and eustachian tube orifice and done more often in canal wall down situations. • Handle of malleus present: In canal wall up procedure, a major columella reconstruction can be done between the footplate and handle of malleus. Cartilage interposition between the TM and columella is done to prevent extrusion. The total ossicular replacement prosthesis (TORP) or graft material can be placed between the footplate of stapes and the handle and neck of malleus. • Handle of malleus absent: When canal wall is intact or has been reconstructed and the major columella TORP is done from the footplate to the cartilage graft.

Type V Tympanoplasty Type V tympanoplasty is done when the stapes footplate is fixed and always done in a staged manner. In the first stage, any middle ear disease is removed and a TM grafting is done and subsequently 6–12 months later, the following procedures may be done. Type Va involves grafting over a fenestration created in the horizontal semicircular canal. This technique has largely been abandoned in favor of the type Vb which involves a stapedectomy.

Type VI Tympanoplasty Sono inversion, where all ossicles absent except footplate of stapes, the round window is exposed and the oval window and eustachian tube area are covered with fascia. This procedure is not done presently as surgeon chooses to do type IV major columella or Vb.

CONCLUSION The procedures that aim at repairing the tympanic membrane have always been considered as the easiest ones in otology. The major goals of tympanoplasty are to reduce the number of infections and improve hearing. Classification of the tympanoplasties on the basis of the defects in the ossicles gives an objective idea of the method of reconstruction and for reporting results.

REFERENCE 1. Merchant SN, McKenna MJ, Rosowski JJ. Current status and future challenges of tympanoplasty. Eur Arch Otorhinolaryngol. 1998;255(5):221-2.

16

Local Anesthesia for Middle Ear Surgery L Paul Emerson, Anand Job

INTRODUCTION Local anesthetics reversibly block nerve conduction. They act by membrane stabilization and decrease the rate of depolarization and repolarization by binding to sodium channels inhibiting sodium influx in the neuronal cell membrane.1,2 These drugs bind more readily to sodium channels in an activated state and thereby onset of neuronal blockade is faster in rapidly firing neurons. They primarily block the sensation of sharp pain, but pressure sensation can still be appreciated. In the absence of inflammation, the mastoid bone is devoid of sensation except for its outer periosteum and to a lesser degree, its inner mucoperiosteum. The advantages of performing middle ear surgery under local anesthesia and conscious sedation include less bleeding, ability to test hearing restoration during surgery, less pain in the immediate postoperative period, early mobilization and cost effectiveness.

PREMEDICATION Atropine of 0.6 mg and 50 mg of pethidine hydrochloride is administered by intramuscular injection 1½ hours prior to surgery.

Sedation in the Operating Room If the patient continues to be apprehensive in the theater, despite the premedication, additional sedation is given. Sedatives reduce patient anxiety and increase patient cooperation. Some of the adverse effects of local anesthetic use, such as apprehension, tachycardia and tremor, may be caused by adrenaline, which can be counteracted by using sedation. This makes the procedure easier and safer to perform. Midazolam IV Adult: 0.5–2 mg onset of sedation 2–3 minutes Diazepam IV Adult: 5–10 mg onset of sedation 5–10 minutes

Injectable Local Anesthetics Lidocaine (Lignocaine) Lidocaine is the most commonly used and least expensive agent. The usual total dose that can safely be given is 3–5 mg/kg. The anesthetic becomes effective 5–10 minutes after infiltration and lasts on average from 45 minutes to 1 hour.3

Local Anesthesia for Middle Ear Surgery 85

Bupivacaine (Marcaine) Bupivacaine is a longer acting agent than lidocaine. The usual total dose that can safely be administered at one time is 2.0–3.0 mg/kg. Bupivacaine takes 10–15 minutes to become effective, which is slightly longer than lidocaine, but its effect lasts for 2–4 hours. If both lidocaine and bupivacaine are mixed together in equal parts and administered, the combination has the added advantages of quicker onset of anesthesia from lidocaine with longer duration of action of bupivacaine.4,5

Additives Bicarbonate: Both lidocaine and bupivacaine are acidic and therefore, painful when injected. To lessen this pain, injectable sodium bicarbonate can be added to the local anesthetic solution.6 • Lidocaine: 1 mL of bicarbonate is added to each 9 mL of lidocaine. • Bupivacaine: 1 mL of bicarbonate is added to each 19 mL of bupivacaine.

Dihydroxyphenyl Methylaminoethanol (Epinephrine or Adrenaline) Adrenaline is a vasoconstrictor and when used with the local anesthetic, reduces bleeding from the surgical site giving a relatively dry surgical field, thus allowing surgery to be performed safely and effectively. Adrenaline also decreases the absorption of the anesthetic agent, thereby permitting safe injection of more than the usually recommended amount of the anesthetic agent. Adrenaline requires 5–7 minutes to take effect. The maximum dosage of lidocaine and bupivacaine with adrenaline are as follows: • Lidocaine with adrenaline increases the dose to 7 mg/kg and the effect lasts 90–120 minutes • Bupivacaine with adrenaline, the dosing remains the same at 2.0–3.0 mg/kg, and its effect lasts 2–4 hours (Table 1).

Caution on Infiltration It is quite dangerous to inject the solution directly into an artery. Prior to injecting the solution, the syringe plunger is withdrawn. If blood is obtained, the needle is repositioned and same procedure adopted, avoiding accidental intra-arterial injection and thus preventing any complications.

Table 1  Overview of anesthetic agents: dosage and duration of action Agents

Maximal dose (mg/kg)

Duration of action

Lidocaine plain

3–5

45–60 minutes

Lidocaine with adrenaline

5–7

1.5–2 hours

Bupivacaine plain

2.0–3.0

2–4 hours

Bupivacaine with adrenaline

2.0–3.0

2–4 hours

86  Current Concepts of Otitis Media and Recent Management Strategies As far as possible use a fine needle to reduce the pain. The greater the needle number, the finer the needle. A 23- or 26-gauge needle is preferred and the injection is given slowly to reduce the pain.

Discomfort during Local Anesthesia Yung7 found that most common discomforts reported were noise during surgery and anxiety, followed by dizziness, backache, claustrophobia and earache. Despite these discomforts, 89% of patients said they would opt for local anesthesia for similar operations in the future.

ADVERSE EFFECTS OF LIDOCAINE Adverse drug reactions (ADRs) are rare when lidocaine is used as a local anesthetic and administered correctly. The ADRs are most often encountered during systemic administration.8 Central nervous system (CNS) effects are caused by CNS excitation such as nervousness, circumoral paresthesia, tinnitus, tremor, dizziness, blurred vision, seizures followed by depression. With increasing exposure there is drowsiness, loss of consciousness, respiratory depression and apnea. The cardiovascular side effects include hypotension, bradycardia, arrhythmias and cardiac arrest.9

Overdosage Overdosage with lidocaine can be a result of excessive administration by prolonged use of subcutaneous infiltration anesthesia such as cosmetic surgical procedures. These occurrences have sometimes led to severe toxicity or death.10 Treatment is with intravenous lipid emulsions (used for parental feeding) to reverse the effects of local anesthetic toxicity.11

Insensitivity to Lidocaine Relative insensitivity to lidocaine is genetic. In hypokalemic sensory over­ stimulation, relative insensitivity to lidocaine has been noted in those who also have attention deficit hyperactivity disorder.12 Local anesthetics often do not act in infected tissue. Tissue acidity can impede the development of local anesthesia. The normal pH of the tissue is 7.4 and the solution in the cartridges predominately cationic (acidic). When the solution is injected into the tissue, the alkalinity of the tissue liberates the free base, allowing penetration of the local anesthetic molecule into the lipid-rich nerve. The acidic environment associated with an active infection causes a much lower tissue pH in the vicinity of 5–6, which favors the quaternary water-soluble configuration and the amount of free base is reduced even further, leaving fewer base molecules to penetrate the nerve. Other factors for failure of anesthesia are edema and the increase in inflammation associated with infections. The selection of an anesthetic with a lower pKa such as mepivacaine (pKa 7.7), would most likely provide more effective anesthesia than bupivacaine (pKa 8.1).13 Infected tissue also may also have an increased blood supply and hence more anesthetic may be removed from the area before it can act on the neuron. 

Local Anesthesia for Middle Ear Surgery 87

ADVERSE EFFECTS OF BUPIVACAINE These are similar to other amide-type local anesthetics, which include lidocaine and are mentioned above.

CONCLUSION Local anesthesia has considerable advantages as compared with general anesthesia. Employment of local anesthesia does not present any disadvantages for the surgeon and the procedure appears to be acceptable for the majority of patients. Patients should be assessed meticulously preoperatively by the surgeon so that it is not performed in unsuitable patients.

REFERENCES 1. Covino BG, Vassalo HG. Local Anesthetics: Mechanisms of Action and Clinical Use. Grune and Stratton. 1976. 2. Strichartz GR, Ritchie JM. Local Anesthetics. Berlin: Springer; 1987. pp.21-52. 3. Tetzlaff JE. The pharmacology of local anesthetics. Anesthesiol Clin North America. 2000;18(2):217-33. 4. Ribotsky BM, Berkowitz KD, Montague JR. Local anesthetics. Is there an advantage to mixing solutions? J Am Podiatr Med Assoc. 1996;86(10):487-91. 5. Sweet PT, Magee DA, Holland AJ. Duration of intradermal anaesthesia with mixtures of bupivacaine and lidocaine. Can Anaesth Soc J. 1982;29(5):481-3. 6. Brogan GX Jr, Giarrusso E, Hollander JE, et al. Comparison of plain, warmed, and buffered lidocaine for anesthesia of traumatic wounds. Ann Emerg Med. 1995;26(2):121-5. 7. Yung MW. Local anaesthesia in middle ear surgery: survey of patients and surgeons. Clin Otolaryngol Allied Sci. 1996;21(5):404-8. 8. Jackson D, Chen AH, Bennett CR. Identifying true lidocaine allergy. J Am Dent Assoc. 1994;125(10):1362-6. 9. Rossi S (Ed). Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook; 2006. 10. Baselt R. Disposition of Toxic Drugs and Chemicals in Man, 8th edition. Foster City, CA: Biomedical Publications; 2008. pp.840-4. 11. Picard J, Ward SC, Zumpe R, et al. Guidelines and the adoption of ‘lipid rescue’ therapy for local anaesthetic toxicity. Anaesthesia. 2009;64(2):122-5. 12. Hakim AJ, Grahame R, Norris P, et al. Local anaesthetic failure in joint hypermobility syndrome. J R Soc Med. 2005;98(2):84-5. 13. Malamed S. Handbook of Local Anesthesia, 6th edition. St. Louis.

17

Approaches for Tympanoplasty L Paul Emerson, Anand Job, John Mathew

INTRODUCTION The approaches for tympanoplasty depends on the anatomy of the external auditory canal and the site of perforation. This chapter provides an overview of the approaches used and management.

TRANSCANAL APPROACH FOR MYRINGOPLASTY In this approach, there is no external incision. It is used for repairing small central perforations limited to one quadrant, small residual perforations, traumatic perforations or where there is a wide ear canal with a posterior perforation and the ear has remained dry (inactive stage). The entire margins should be clearly visualized. Sometimes anterior perforations are difficult to address by this method as the anterior margin may often be obscured by an overhanging anterior canal wall. Self-retaining specula allows for a bimanual procedure and is an advantage during surgery. Local anesthesia should be carefully injected to avoid bulging of the external auditory canal so that there is adequate vision of the perforation and remnant tympanic membrane.

ENDAURAL APPROACH In the endaural approach, an incision is made between the tragus and helix to obtain exposure and the entrance to the ear canal is then stretched open with endaural retractors. Most central perforations can be managed using this approach and is a good approach for posterior perforations. While the view is superior to a transcanal approach, it sometimes is not suited for anterior perforations especially if there is an anterior canal bony overhang. Enlargement of the ear canal and the partial reduction of a prominent anterior canal wall to expose the anterior part of the tympanic membrane may be necessary. Additionally, tragal cartilage or perichondrium can easily be harvested by extending the incision to the anterior portion of the external meatus. If simple mastoidectomy is required, the postauricular approach gives a better exposure.

RETROAURICULAR APPROACH Retroauricular approach is used in most situations when surgery of the mastoid is also expected. This approach is preferable for assessment of the sinodural angle, air cells behind the sigmoid sinus and the potentially pneumatized posterior portion of the zygomatic arch.

Approaches for Tympanoplasty  89

Retroauricular Approach Incision The postaural incision is made just behind the postaural sulcus or on the hair line for an invisible scar and the soft tissue, and pinna is reflected anteriorly. Although favored for anterior perforations as it provides an improved angle of vision for the anterior rim, any perforation can be closed by this approach and the mastoid can also be addressed.

Canaloplasty A circumferential canaloplasty can be done in cases where there is a significant anterior and posterior bony overhang. Posterior canaloplasty is done after elevating the tympanomeatal flap and the posterior bony annulus is curetted along with the bony overhang. This also reduces the potential of the ossicular prosthesis fixation to the canal wall.

Harvesting the Graft (Temporalis Fascia) Temporalis fascia consists of a superficial and a deep layer. The deep layer is used for grafting as it is thicker and more resilient. The fascia can be harvested at the end of the procedure as the surgeon knows how much fascia is required as sometimes revision surgery may be required. An assistant exposes the fascia by superiorly retracting skin and soft tissue with a Langenbeck retractor (Fig. 1). A transverse incision is made in the deep layer of fascia parallel to linea temporalis with a No. 11 blade. The undersurface of the fascia is undermined

Fig. 1  Exposing temporalis fascia

90  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 2  Excision of temporalis fascia graft

through this incision and separated from the temporalis muscle with scissors and harvested (Fig. 2). The fascia graft is compressed between two gauze swabs, but not dried. Using No. 10 blade, the graft is scraped clean of muscle fibers. Uneven edges are trimmed with a No. 10 blade. An incision is made in the flap with a knife to accommodate the tensor tympani tendon at the anticipated location of the malleus handle.

Harvesting Tragal Cartilage and Tragal Perichondrium Tragal cartilage is easily harvested by exposing the upper end of the tragal cartilage through an endaural approach. The tragal cartilage is held with surgical forceps, while dissecting the soft tissue off the cartilage with tympanoplasty scissors. After exposing the amount of cartilage required for reconstruction, cartilage is resected with overlying perichondrium with tympanoplasty scissors. Perichondrium can be left intact or removed as per the preference of the surgeon. The cartilage can be thinned using a No. 10 blade.

Surgical Steps of Endaural Approach Infiltration of the endaural skin incision as well as the ear canal in four quadrants is done with local anesthetic (lidocaine 1% and adrenaline diluted to 1:200,000), using an ear speculum to expose the ear canal. A skin incision is made in the bony external canal with a No. 15 blade from the 12 o’clock position, spiraling upwards between the cartilages of the helix of the pinna and tragus (Fig. 3). An incision of 1.5 cm in length is made extending down to the bone. Using a No. 11 blade, a skin incision is made in the posterior aspect of the bony external canal parallel to the annulus, starting at 8 o’clock (for right ear) and ascending in a spiral fashion to

Approaches for Tympanoplasty  91

Fig. 3  Endaural incision at 12 o’clock

Fig. 4  Posterior canal incision that meets endaural incision

meet the endaural incision at 12 o’clock (Fig. 4). An elevator is used to reflect the canal skin and soft tissue laterally and away from the edges of the tympanomeatal flap (Fig. 5). An incision is made anteriorly in the bony canal skin, parallel to the annulus keeping medial to the aural canal cartilage. It starts at 2 o’clock and meets the endaural skin incision at 12 o’clock (Fig. 6).

92  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 5  Reflecting canal skin anteriorly

Fig. 6  Anterior incision starting at 2 o’clock

Two endaural retractors are next placed in the ear canal to improve exposure (Fig. 7). The edges of the perforation are freshened using a curved pick and then the tympanomeatal flap is elevated using a canal elevator.

Approaches for Tympanoplasty  93

Fig. 7  Placement of retractors

Fig. 8  Elevating the tympanomeatal flap

If a prominent tympanosquamous suture prevents good exposure, then it is drilled using a 2.7 mm diamond drill. To avoid bone dust from entering the middle ear, gel foam is placed into the perforation. The middle ear is entered by elevating the tympanomeatal flap at the level of the posterior tympanic spine (Fig. 8). The annulus starts at this level and can be easily dissected free of its sulcus using a

94  Current Concepts of Otitis Media and Recent Management Strategies stapes knife. The chorda tympani immediately beneath the tympanic spine is identified and preserved. The posterior tympanic spine and bone of the posterior canal wall is curetted until the incus, incudostapedial joint, lateral process of the malleus and round window are visible. Using a 1.5 mm, 45° hook the ossicles are palpated for mobility. Depending on the ossicular chain, ossiculoplasty and tympanoplasty is done as an underlay graft beneath the edges of the perforation. Gelfoam is avoided in the middle ear if there are areas of mucosal necrosis and denuded epithelium, and silastic sheet is employed to prevent graft medicalization and fibrosis. Posteriorly and superiorly it is laid onto the bony canal lateral to the posterior tympanic sulcus. The tympanomeatal flap is returned to its original position and gelfoam pledgets placed over the graft to secure it over the posterior tympanic sulcus. The endaural skin incision is closed with 3.0 Nylon sutures.

Surgical Steps of Postaural Approach Using local anesthetic (lidocaine 1% and adrenaline diluted to 1:200,000), the postauricular sulcus is infiltrated. The needle is advanced to infiltrate the tissues anteroinferiorly and anterosuperiorly. Using a Lempert speculum, the bony-cartilaginous junction of the ear canal is injected at the four quadrants of the skin of the ear canal (Fig. 9). A postauricular incision is made about 0.5 cm behind the retroauricular sulcus extending from the upper border of the pinna to the level of the mastoid tip. Light cross hatchings are made with a scalpel before incising the skin, to facilitate aligning the skin when closing the wound. Using a periosteal elevator the pinna is retracted anteriorly. As the flap is developed the posterior auricular muscle is encountered and transected. Superiorly, the temporalis fascia comes into view (Fig. 10). The fascia can be harvested now or later.

Fig. 9  Points of injecting ear canal

Approaches for Tympanoplasty  95

Fig 10  Temporalis fascia and retroauricular periosteal flap

An anteriorly based retroauricular periosteal flap is now developed. A vertical incision is made approximately 1.5 cm from the ear canal reaching the linea temporalis (Fig. 10). Using a No. 10 blade, a superior incision is made extended anteriorly along the linea temporalis up to 12 o’clock relative to the bony ear canal. The inferior incision is extended to the inferior border of the ear canal. A periosteal flap is elevated from the bone with a mastoid elevator until Spine of Henlé and the bony external canal up to the 12 o’clock position, are exposed. The meatal skin flap is raised. The periosteal flap is elevated up to about 2 mm deep to the lateral edge of the bony external ear canal. Using No. 11 blade, the ear canal is entered via a transverse incision in the posterior ear canal skin at about the middle at 9 o’clock (right ear). The lumen of the ear canal is then visible through the incision (Fig. 11). Using a scalpel a cut is made in a cephalad direction extending superiorly up to 12 o’clock (Figs 12 and 13). An incision is made in the skin of the superior and anterior wall of the ear canal starting at 12 o’clock and extended anteriorly to 3 o’clock (Figs 13 and 14). This incision runs lateral to the tympanosquamous suture line and also has to remain on bone and medial tragal cartilage; if the incision is placed too laterally then the tragal cartilage will be injured. Using a Lempert periosteal elevator, the lateral canal skin is elevated from the underlying bone (Figs 15 and 16). The pinna and soft tissue are reflected forward. Two self-retaining retractors are placed superiorly and inferiorly and used to reflect the soft tissue and improve exposure. The meatal skin is now further incised anteroinferiorly from 3 o’clock to 5 o’clock (Fig. 16). The incision spirals laterally and superiorly along the anterior canal wall to meet the earlier incision made in the anterior canal at 3 o’clock (right ear). The skin should be fully cut onto the bone to prevent flap tear when elevating it with the microraspatory. The meatal skin flap is circumferentially elevated from the underlying bone with a periosteal elevator. To keep this dissection blood-free and to avoid

96  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 11  Incising posterior ear canal

Fig. 12  Incisions for spiral flap technique

injuring the skin flap, adrenaline-soaked gauze is placed between the Lempert’s microraspatory and the meatal skin. Suction is never directly applied to the meatal skin flap; rather the excess blood is suctioned through the adrenalinesoaked gauze. The blade of the Lempert’s microraspatory stays vertical to the

Approaches for Tympanoplasty  97

Fig. 13  Posterior incision extended as spiral incision to anterior canal wall till 3 o’clock

Fig. 14  Incising anterior canal

bone and the shoulder of the instrument is used to push against the adrenaline gauze, which then atraumatically elevates the very fragile meatal skin (Figs 16 and 17). The meatal skin is elevated until the posterosuperior margin of the tympanic membrane and the anteroinferior overhang of bone are exposed.

98  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 15  Elevating skin from bone

Fig. 16  Completing incision in anterior canal wall

At the tympanosquamous suture line (located posterosuperiorly) the skin flap is very tightly bound to the underlying bone and may be dissected free using the raspatory. Any soft tissue connection to the suture is cut with Bellucci scissors. Using No. 11 blade the posterior limb of the meatal skin flap is incised 2 mm lateral and parallel to the annulus (see Figs 4 and 18).

Approaches for Tympanoplasty  99

Fig. 17  Elevating meatal skin

Fig. 18  Incise posterior limb of meatal skin flap 2 mm lateral to and parallel to the annulus

Bellucci scissors is then used to continue incising the meatal skin flap 2 mm lateral to and parallel to the annulus until the anterior part of the flap is reached (Fig. 18). The remaining meatal skin is transected to 6 o’clock, 2 mm lateral to the annulus, using an Iowa raspatory or a round knife (Fig. 19).

100  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 19  Transect remaining meatal skin to 6 o’clock, 2 mm lateral to the annulus

Fig. 20  Flap pedicled inferiorly and elevated from canal wall

Using the Lempert raspatory the meatal skin lateral to this circumferential incision is dissected free from the bony canal. Using a bigger instrument avoid injuring the inferiorly based pedicle (Fig. 18). Elevate the lateral aspect of the anterior meatal skin flap with a key raspatory and using two hands, advance the raspatory over the lateral rim of the tympanic bone (Fig. 20). Once the lateral

Approaches for Tympanoplasty  101

Fig. 21  Soft tissue is elevated out of the bony external canal

Fig. 22  Ribbon passed around meatal spiral flap

edge of the tympanic bone is reached, keep the tip of the instrument in contact with the bone and underlying tissue, but swing the handle of the Key raspatory anteriorly so that the soft tissue is elevated out of the bony external canal, leaving it pedicled inferiorly (Figs 20 and 21). The spiral of elevated meatal skin is kept out of the surgical field by using ribbon gauze passed around the meatal skin flap (Fig. 22). The ribbon is folded back over the top of the retractor.

102  Current Concepts of Otitis Media and Recent Management Strategies

CONCLUSION Each of the approaches for tympanoplasty has its own advantages and limitations. The incision selected for tympanoplasty should be determined by the location of the perforation and extent of disease in the middle ear and mastoid. The anterior external endaural incision allows direct exposure of temporalis fascia, the external meatus, bony canal and perforation involving the posterior tympanic membrane and ossicular chain. The postauricular incision gives direct exposure of the anterior tympanic membrane with preservation of the anterior canal wall skin. The transmeatal approach should be reserved for smaller central perforations which does not require mastoidectomy.

BIBLIOGRAPHY 1. Farrior JB. Incisions in tympanoplasty: anatomic considerations and indications. Laryngoscope. 1983;93(1):75-86. 2. Mirko Tos. Manual of Middle Ear Surgery, Volume 2: Mastoid Surgery and Reconstructive Procedures. Leipzig, Germany: Thieme medical publishers; 1995.

18

Surgery of Tympanoplasty Anand Job, L Paul Emerson, John Mathew

MYRINGOPLASTY Myringoplasty is similar to type I tympanoplasty, except no tympanomeatal flap is elevated to inspect the middle ear. When there is a very small perforation of one quadrant only, then the graft can be placed by underlay technique without elevating a tympanomeatal flap, after freshening the margins of the perforation and making a raw area under the remnant of the tympanic membrane (TM). Fat can also be used as graft material, in very small perforations. This procedure is most commonly done when a perforation fails to heal following grommet extrusion.

TYPE I TYMPANOPLASTY In type I tympanoplasty, the middle ear and ossicles are inspected and disease eradicated if present, prior to graft placement.

Surgical Technique The standard technique is to elevate a tympanomeatal flap from 12 o’clock to 6 o’clock, examine the middle ear and place the temporalis fascia by underlay technique, the flap providing the vascularity to the graft.

Swing Door Technique of Palva In the swing door technique of Palva, the tympanomeatal flap is elevated as a superior and inferior based flap, after making a transverse cut at the 9 o’clock position.

Factors Affecting Surgical Outcome Autologous temporalis fascia graft remains the preferred graft material for its superior tissue quality, of easy availability and low basal metabolic rate (BMR). Many studies have been carried out in the past regarding structural and functional outcomes following type I tympanoplasty by utilizing temporalis fascia using the underlay technique. The quoted success rate in various studies ranged from 80% to 95%. Palva1 reported 97% success of TM repair and air-bone gap of less then 20 dB in 69% of patients. The most frequent causes of immediate graft perforations are technical in nature, such as perioperative bleeding or the use of a graft that is too small.

104  Current Concepts of Otitis Media and Recent Management Strategies During the later postoperative period, chronic sinusitis was the most significant factor associated with graft reperforation. Postoperative infection, residual perforation, dislodgement of graft, anterior blunting, retraction pockets and damage to chorda tympani are the common complications.2 Graft failures can also occur because of inadequate packing of the anterior mesotympanum with gel foam. The graft success rate is high in traumatic perforation of the TM, due to presence of normal healthy middle ear mucosa. Other factors commonly related to successful outcome are size and site of perforation, duration of discharge and associated pathology in the middle ear.3

Additional Risk Factors in Children Age less than 8 years was found to be a poor prognostic factor by Black et al4 and MacDonald et al.5 Reasons cited for poor results are—immaturity of eustachian tube function, high incidence of recurrent upper airway infections, otitis media with effusion, adenoiditis and surgical difficulty presented by a narrow external auditory canal in children. Middle ear gas volume of less than 3 mL is a poor prognostic factor for TM graft closure in children.6 Middle ear pathologic findings in the contralateral ear, suggesting tubal dysfunction was also a predictor for reperforation and retraction. For many reasons, better success has been noted when cartilage has been used.

TYPE II TYMPANOPLASTY Type II tympanoplasty is done for minor ossicular defects.

Group 1 Tympanoplasty with Malleus Handle Eroded (Fig. 1) Several techniques have been adopted to replace the handle of malleus to improve hearing results, although reproducing the catenary lever has not been possible. The Sheehy technique uses tragal cartilage placed on to the intact remaining ossicular chain. A long cartilage plate is placed from under the posterosuperior bony annulus in an anteroinferior direction, on to the incudostapedial joint. Temporalis fascia is used to cover the TM defect, cartilage graft as well as the malleus remnant. Alternatively, a composite cartilage-perichondrium graft can be used in a similar fashion. Also, the cartilage palisade technique can be used to cover the malleus remnant and TM defect.

Group 2 Tympanoplasty with Incus Eroded • Subtype 1: The lenticular process is necrosed and needs to be bridged (Fig. 2). • Subtype 2: Long process necrosed and incus interposition or a suitable prosthesis is needed (Fig. 3). • Subtype 3: Entire incus in necrosed and prosthetic interposition is needed (Fig. 4).

Surgery of Tympanoplasty 105

Fig. 1  Tympanoplasty with malleus handle eroded

Fig. 2  Tympanoplasty with incus eroded (subtype 1)

There are varying degrees of incus necrosis and the reconstruction involves repositioning the incus or to bridging the small defect, keeping the incus without disarticulation or to replace the incus with cartilage, bone or prosthetic material partial ossicular replacement prosthesis (PORP). Most commonly used material is autologous incus followed by cortical bone, malleus head, tragal cartilage, conchal cartilage and biocompatible materials PORP. Allogeneic grafts are no longer popular due to biosafety issues.

106  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 3  Tympanoplasty with incus eroded (subtype 2)

Fig. 4  Tympanoplasty with incus eroded (subtype 3)

Incus Used for Interposition Disadvantages • Prolonged operative time • Displacement • Complete resorption • Possibility of autograft harboring microscopic cholesteatoma • Disease process may have eroded available ossicles • Poor fit, if the stapes superstructure is absent.

Surgery of Tympanoplasty 107 Advantages • Low extrusion rate • No risk of transmitting disease • Low cost • Biocompatibility • No necessity for reconstitution • Fully biocompatible. The approach is transcanal as described by Guilford. The stapes and long process remnant are exposed adequately by drilling the posterosuperior canal wall and bony annulus, similar to stapedectomy approach. The incus remnant is dislocated from the malleus and rotated and taken out carefully, taking care not to dislodge the stapes. The body of incus is now placed on the head of stapes and the short process points anteriorly and placed in contact with the undersurface of the handle of malleus. The chorda tympani can be placed over the body of incus, to stabilize the reconstruction. Sometimes the graft may need to be placed over the handle of malleus (over-underlay), so as to not destabilize the reconstruction. Incus interposition is done when the angle between the long axis of the stapes capitulum and malleus handle is favorable (preferably < 30°). Angles more than 45° prevent proper sound transfer between the stapes and malleus. Some sound energy is converted into an inefficient rocking motion at the footplate if the manubrium is too far, anterior to the stapes. In such instances when it is found that the malleus handle is retracted and anterior, it is corrected by gently retracting the handle laterally and posteriorly. If it is necessary to cut the tensor tympani tendon, pull the malleus backwards to sever the anterior malleolar ligament, for better results. Then the incus is interposed. Head of malleus can also be shaped when incus is absent. A socket can be made in the neck for the stapes head and a groove on the head, to fit the handle of malleus.

Cartilage Cartilage was first used by Utech in 1959 and can be easily harvested from the tragus and interposed in the defect. Sometimes two pieces may have to be placed one over the other between the stapes head and handle of malleus.

Group 3 Tympanoplasty with Stapes Superstructure Eroded • Subtype 1: Medial defect; defects of the stapes arch with head and neck present (Fig. 5). • Subtype 2: Lateral defect; absent head and neck or lateral part of the arch (Fig. 6). For medial defects, bone can be fashioned to fit the minor defect. For lateral defects, the incus can be disarticulated, refashioned and interposed.

TYPE III TYMPANOPLASTY The stapes alone is intact (Fig. 7). In a canal down situation, the graft can be placed on the stapes head, the reconstruction being known as collumella effect. It has been observed that the hearing results can be often acceptable.

108  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 5  Tympanoplasty with stapes superstructure eroded [subtype 1 (medial defect)]

Fig. 6  Tympanoplasty with stapes superstructure eroded [subtype 2 (lateral defect)]

However, if the canal is intact, placing the graft on the stapes head is difficult and can result in retraction pockets and cholesteatoma later. Hence, most surgeons prefer to reconstruct by using a minor columella from stapes head to TM. Cartilage and bone interpositions (carved incus or cortical bone) between the stapes head and TM is done to improve hearing results. In the Heermann technique, a long strip of cartilage is used from the annulus at 6 o’clock to the stapes head.

Malleus Head Fixation Malleus head fixation occurs in the epitympanum. Two different approaches can be used. Using a transmastoid approach without disruption of the ossicular

Surgery of Tympanoplasty 109

Fig. 7  Type III tympanoplasty (stapes alone is intact)

chain or transcanal approach, the malleus head is removed with the incus and reconstructed by incus interposition or by PORP.

REFERENCES 1. Palva T. Surgical treatment of chronic middle ear disease. Myringoplasty and tympanoplasty. Acta Otolaryngol. 1987;104(3-4):279-84. 2. Emir H, Ceylan K, Kizilkaya Z, et al. Success is a matter of experience: type 1 tympanoplasty: influencing factors on type 1 tympanoplasty. Eur Arch Otorhinolaryngol. 2007;264(6):595-9. 3. Ashfaq M, Aasim MU, Khan N. Myringoplasty: anatomical and functional results. Pak Armed Forces Med J. 2004;54(2):155-8. 4. Black JH, Hickey SA, Wormald PJ. An analysis of the results of myringoplasty in children. Int J Pediatr otorhinolaryngol. 1995;31(1):95-100. 5. MacDonald RR 3rd, Lusk RP, Muntz HR. Fascia form myringoplasty in children. Arch Otolaryngol Head Neck Surg. 1994;120(2):138-43. 6. Sade J. The atelectatic ear. In: Sade J (Ed). Monograms in Clinical Otolaryngology, Secretory Otitis Media and its Sequelae. New York, Churchill-Livingstone; 1979. pp. 64-88.

19

Tympanic Membrane Reconstruction Using Cartilage Anand Job, L Paul Emerson, John Mathew

INTRODUCTION Cartilage tympanoplasty achieves good anatomical and audiological results. In cases of subtotal perforations, atelectatic ear, retraction pocket, ossiculoplasty or mastoid surgery, long-term results of temporalis fascia graft may not be very satisfactory. Cartilage contributes minimally to inflammatory tissue reaction and is well incorporated with tympanic membrane (TM) layers. It also provides firm support to prevent retraction. The greatest advantage of the cartilage graft has been thought to be its very low metabolic rate. It receives nutrients by diffusion and is easy to work with because it is pliable and it can resist deformation from middle ear pressure variations. Cartilage tympanoplasty1 achieves good results when pathology and status of the ossicular chain dictate the technique utilized. Significant hearing improvement was realized in each pathological group. In the atelectatic ear, cartilage allowed reconstruction of the TM with good anatomic results compared to traditional reconstructions, which have shown high rates of retraction and failure. In cholesteatoma, cartilage tympanoplasty using the palisade technique resulted in precise reconstruction of the TM and helped reduce recurrence. In cases of high-risk perforation, reconstruction with cartilage yielded anatomical and functional results that compared favorably to primary tympanoplasty using traditional techniques.

CLASSIFICATION OF CARTILAGE TYMPANOPLASTY Tympanoplasty using cartilage can be broadly classified into three classes depending on the shape and the thickness of the cartilage as well as the perichondrial covering. Various techniques have been used to reconstruct the TM.

CLASS I Palisades Technique Cartilage palisades of 0.5–3 mm wide are placed side by side, under the eardrum remnant, usually in a superoinferior direction, but can be placed in anteroposterior or in oblique direction as well. Heermann2,3 placed the anterior palisade under the anterior bony annulus. The superior end is supported by a piece of cartilage, placed on to the eminence of the tensor tympani muscle. Inferiorly and posteriorly the palisades are placed on to the bony annulus (Fig. 1).

Tympanic Membrane Reconstruction Using Cartilage 111

Fig. 1  Underlay cartilage palisade tympanoplasty in a total perforation

Fig. 2  Palisades are placed at the level of the bony annulus

Another modification is placement of the palisades at the level of the bony annulus (Fig. 2) and a third modification is by placing all the cartilage palisades under the bony annulus (Fig. 3). Six to eight palisades are required to close a total perforation.

112  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 3  All palisades are placed under the bony annulus

Fig. 4  Two broad and a small short palisade cover as underlay grafts the total perforation

Tympanoplasty with Broad Cartilage Palisades When 4–5 mm broad palisades are used, only two or three palisades are needed to cover a total perforation. The palisades are placed as underlay grafts (Fig. 4).

Tympanic Membrane Reconstruction Using Cartilage 113

Oblique Palisade The cartilage can be cut in an oblique manner and the pieces are placed like roof tiles. The edge of the next stripe is placed on to or under the edge of the previous stripe.

CLASS-II Jigsaw Technique Dornhoffer Cartilage Mosaic Tympanoplasty1,4 The full-thickness slices or pieces of cartilage are pieced together, like the pieces of a jigsaw puzzle, to reconstruct a total perforation (Fig. 5). In contrast to the strict Heermann technique, this Dornhoffer mosaic technique is more liberal, allowing slices of various shapes and sizes. Cartilage is cut into foils, thin plates or thick plates and denuded of perichondrium. These serve as reinforcement of the remnant eardrum or temporalis fascia. The foils are 0.2–0.3 mm thick and overlap each other, like the leaves of a tulip blossom. The plates are of variable thickness from 0.5–1.0 mm, and are positioned either at the level of the bony annulus or on to the posterior bony annulus (Fig. 6).

Fig. 5  Full-thickness slices or pieces of cartilage are pieced together, like the pieces of a jigsaw puzzle

114  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 6  Three cartilage foils are placed under the denuded eardrum remnant the second foil is overlapping the first and the third foil

CLASS-III Tympanoplasty with Cartilage-Perichondrium Composite Island Grafts Cartilage-Perichondrium Composite Island Graft Tympanoplasty The total island graft with a diameter of 7–9 mm is used to close a total or subtotal perforation. There are four modifications (Figs 7A to D): 1. The round graft. 2. The round graft with a wedge to accommodate the malleus handle. 3. The Dornhoffer graft,4,5 consisting of two semicircular disks, connected by perichondrium. 4. Jahnke graft,5 with four cartilage belts.

Posterior Cartilage-Perichondrium Composite Island Graft Tympanoplasty 6 This graft has a rectangular or oval, full-thickness cartilage disk and a large posterior perichondrium flap, placed on to the posterior ear canal wall. It is useful in closure of a posterior perforation and the ossiculoplasty can be done concurrently (Fig. 8).

Tympanic Membrane Reconstruction Using Cartilage 115

B

A

C

D

Figs 7A to D Cartilage-perichondrium composite island graft tympanoplasty: (A) The round graft; (B) The round graft with a wedge to accommodate the malleus handle; (C) The Dornhoffer graft, consisting of two semicircular disks, connected by perichondrium; (D) Jahnke graft with four cartilage belts

Fig. 8 The cartilage disk is positioned under the eardrum remnant; the posterior perichondrium flap is placed on to the ear canal bone, the anterior flap under the malleus handle and anterior part of the eardrum

116  Current Concepts of Otitis Media and Recent Management Strategies

REFERENCES 1. Dornhoffer JL. Cartilage tympanoplasty: indications, techniques, and outcomes in a 1,000-patient series. Laryngoscope. 2003;113(11):1844-56. 2. Heermann J Jr., Heermann H, Kopfstein E. Fascia and cartilage palisade tympanoplasty. Nine years’ experience. Arch Otolaryngol. 1970;91(3):228-41. 3. Heermann J. Autograft tragal and conchal palisade cartilage and perichondrium in tympanomastoid reconstruction. Ear Nose Throat J. 1992;71(8):344-9. 4. Dornhoffer JL. Cartilage tympanoplasty. Otolarygol Clin North Am. 2006;39(6):116176. 5. Jahnke K. [Biomechanics of the reconstructed ear ossicular chain]. HNO. 1998;46(3): 202-4. 6. Linde RE. The cartilage-perichondrium graft in the treatment of posterior tympanic membrane retraction pockets. Laryngoscope. 1973;83(5):747-53.

20

Ossicular Reconstruction John Mathew, Anand Job, L Paul Emerson

INTRODUCTION It is over 40 years since incus repositioning was first performed with homograft and autograft incus for necrosis of the long process. This method proved to be consistently successful and is one of the commonly done ossiculoplasties due to the stability offered by the head of stapes and handle of malleus. Failures encountered are due to dislocation of the interposed incus, fusion to the posterior bony canal wall and resorption. However, similar results could not be obtained when incus was used to reconstruct from the stapes footplate to the handle of malleus, although due to stiffness of the bone graft and fusion to the malleus and to the stapes footplate with perpendicular action, good sound transmission was expected. It was later realized that failures were due to inadequate length and too wide for the narrow oval window niche with poor hearing results, and also displacement at the footplate junction or bone-bone fusion laterally between the bone graft and the medial external auditory canal. Use of homografts required special banks that might not be widely available and also lost popularity as possible infectious transmissions could not be ruled out. Also, biological materials, such as bone and cartilage present disadvantages such as resorption and extended surgical time for sculpting. Allograft incus also had the risk of reimplantation of cholesteatoma. Cartilage has also been tried and found successful for reconstructions between the malleus handle and head of stapes, but between the footplate of stapes and handle of malleus, due to the added length of reconstruction, over time it tends to become soft and eventually becomes bent with poor hearing. The results of ossiculoplasty were 40–70% in patients with an intact stapes and 20–55% in those with only footplate.1–5

PORP AND TORP IN OSSICULOPLASTY Hearing results using prosthetic implants were expected to yield better results than cartilage and bone. However, this did not happen, especially with total ossicular replacement prosthesis (TORP)s due to instability and dislocation, which are inherent risks associated with total middle ear ossicular reconstruc­ tions with absent incus and missing stapes arch. During surgery, additional complications arose due to each patient’s unique anatomical features, which often made it difficult and cumbersome to achieve an optimal connection with the stapes footplate with results not being consistent. Hence, a wide range of

118  Current Concepts of Otitis Media and Recent Management Strategies prosthetic designs and materials were developed for ossicular reconstruction, to optimize postoperative functional results. (Figs 1 and 2).

Fig. 1  Duesseldorf titanium prosthesis AERIAL (total)

Fig. 2  Duesseldorf titanium prosthesis

Ossicular Reconstruction 119 The ideal prosthesis for ossicular reconstruction should be stable, safe, easily insertable and capable of yielding optimal sound transmission. Selection of a particular prosthesis must also be based on biocompatibility and ease of intraoperative configuration during surgery.

Choice of Prosthetic Material Proplast, a combination of two polymers had the advantage of being porous to allow for tissue integration and prevent host graft rejection. The problem was that the shaft, which was made of Teflon and was not amenable to contouring and the prosthesis proved difficult to position. Plastipore, a high density polyethylene sponge and polycel, a thermal-fused form, although had the advantage of allowing contouring, had the distinct disadvantage of fusing with nearby bony structures such as promontory and facial canal. Hydroxyapatite was used in the 1980s and Grote, the first to use this found it biocompatible. Hydroxyapatite is composed of calcium phosphate and is used in a dense or porous state. In the dense state it bonds to bone. Being biocompatible it could be placed directly against the tympanic membrane, but not close to bone and hence was ideally suited to be used as the head piece and not the shaft for prosthesis, thus overcoming the disadvantage and using the advantage. Titanium is a light, but solid material, providing optimal sound transmission, and has been shown to be highly biocompatible. It is nontoxic, nonmagnetic magnetic resonance imaging (MRI) compatible, nonerosive and chemically stable, with low specific density (57% that of stainless steel), and is extremely strong. No macrophages or foreign body reactions were seen in titanium prostheses removed during revision surgery and studied by scanning electron microscopy. Ossicular prostheses made of titanium are among the lightest models, weighing between 4.1 and 10.1 mg.6 The thin design facilitated positioning of the prosthesis especially the lower end allowing good visualization of the foot plate and causing no contact with nearby structures. The light weight had a favorable effect on acoustic properties, with good results in sound transmission in the higher frequencies (3,000–4,000 Hz).7–9 Studies have shown that after implantation, a thin, noninflamed, even layer of epithelium forms over the inserted implant. Titanium forms a biostable titanium oxide layer when combined with oxygen. Also, differential processing of the material surfaces triggered different tissue reactions. Rough-milled surfaces causing more tissue reaction was most appropriate in areas that contacted cartilage or the stapes head or footplate. Conversely, the smoother the surface, less connective tissue reaction occurred and epithelial covering was minimized, being ideal for the shaft of the prosthesis. Prostheses with a titanium head plate required interposition of a cartilage disk between the prosthesis and the tympanic membrane or graft to prevent extrusion, whereas the hydroxyapatite prostheses can be placed directly in contact with the tympanic membrane with no extrusion. Hence, it is an advantage to have prosthesis with a titanium shaft and hydroxyapatite head. In different frequency bands of the same sound pressure, partial ossicular replacement prosthesis (PORP)s with different materials have different effects on hearing restoration. A better sound transmission in low frequencies is obtained

120  Current Concepts of Otitis Media and Recent Management Strategies by PORPs with hydroxyapatite. Also, in the 500–3,000 Hz range, which clinicians measure and pay attention to better sound transmission is gained by PORPs with hydroxyapatite. The hearing restoration value of hydroxyapatite is 7.1 dB larger than that of stainless steel. The hearing restoration value of titanium is 4.9 dB larger than that of stainless steel. Hydroxyapatite ceramics has better effects on sound transmission than titanium and other materials.

GENERAL PRINCIPLES OF RECONSTRUCTION The principles of reconstruction are the two point stabilization technique described by Dornhoffer, free standing chain at the end of procedure, adopting techniques to prevent extrusion and the use of prosthesis, which result in good sound transmission. When reconstructing the ossicular chain, an intact stapes and presence of handle of malleus provide excellent stability to the prosthesis and provide for adequate middle ear space with good hearing results. When the malleus handle is absent, cartilage is the preferred graft material to reconstruct the tympanic membrane, so that the upper end of the prosthesis can be placed on the undersurface of the cartilage to prevent extrusion. In the absence of the stapes superstructure, the lower end of the prosthesis can slip and get dislodged or can make contact with the bony oval window margin and get fixed to it causing a conductive hearing loss. Hence, the lower end of the prosthesis needs to be rough. Compressed areolar tissue is placed over the footplate to cover part of the promontory and facial canal to prevent prosthesis to bone adhesion. The lower end of the prosthesis is then placed over the center of the footplate over the areolar tissue thus stabilizing the prosthesis. Alternatively, a shoe can be kept on the footplate and the lower end inserted into its socket. While performing prosthesis interposition, the angle between the long axis of the stapes capitulum and malleus handle should preferably be less than 30°. Angles more than 45° prevent proper sound transfer between the stapes and malleus, as some sound energy is converted into an inefficient rocking motion at the footplate as the manubrium is too far anterior to the stapes. In such instances when the malleus handle is anterior and retracted, prosthesis insertion is also difficult. This can be overcome by gently retracting the handle laterally and posteriorly. Sometimes, it is necessary to cut the tensor tympani tendon for better results. This maneuver brings the prosthesis more vertical, shifting the center of gravity nearer the footplate, providing better stability. Also, the eccentric head design allows better vertical positioning of the prosthesis, which shifts the center of gravity over the shaft. If the retracted and anterior malleus handle cannot be mobilized adequately, the prosthesis can be placed under the neck of malleus, thus circumventing the abnormal position of the malleus handle. The status of middle ear disease also has an important role in the long term outcomes of ossicular reconstruction. If disease pathology cannot be excised completely, the ossiculoplasty can be staged. Also, when large areas of mucosa have been removed, results with TORPs are not encouraging and the ossiculoplasty will need to be staged. Silastic sheeting in the middle ear may also be needed to prevent fibrosis.

Ossicular Reconstruction 121 Type I tympanoplasty does not require ossicular reconstruction. Type II tympanoplasty (minor ossicular defect) necrosis of lenticular or long process of incus less than 3 mm.

Prosthesis for Bridging up to 3 mm Gap for Incus Necrosis Applebaum hydroxyapatite prosthesis for long process defect less than 3 mm. This hydroxyapatite prosthesis is designed for long process defects and consists of a rectangular piece of hydroxyapatite with a groove through the proximal end extending the length of the rectangle. The groove stops short of penetrating the distal end of the rectangular prosthesis. At this distal end of the groove, a circular hole passes through the floor of the groove. The groove is designed to accommodate the remnant of the incus long process and the circular hole receives the stapes capitulum. The prosthesis is placed by gently lifting the long process of the incus and sliding it into the groove. Then the hole of the prosthesis is placed onto the stapes head. This procedure results in a stable connection requiring no further packing or tissue adhesion (Figs 3 and 4). Advantages of the Applebaum prosthesis are: Bridging defects of up to 3 mm is possible. It does not loosen and continuity is maintained over time. The prosthesis avoids technical difficulty and time involved in constructing bone or cartilage grafts. The incus is retained in original position and the incudomalleal joint is left intact.

A

B

C

D

Figs 3A to D  There is variable rotation of the malleus in a left ear on an axis at a point near the attachment of the anterior malleal ligament and tensor tympani tendon at the neck

122  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 4  Angular clip prosthesis

Type II tympanoplasty: Minor ossicular defect—necrosis of long process of incus, prosthesis for bridging more than 3 mm defect in incus long process. For incus defects over 3 mm bridge type prosthesis of titanium with clip type/ clamp type are useful.

Type II Major Ossicular Defect—Incus Major Erosion or Absent Body of Incus Present Incus Interposition The remnant incus is dislocated from the malleus and interposed between the handle of malleus and stapes head as described in the earlier chapter.

PORP Reconstruction (Fig. 5) The presence of malleus handle and stapes suprastructure provides excellent stability for the PORP and give good hearing results in ossiculoplasty.10,11 Anchoring of the prosthesis to the manubrium of the malleus provides better stabilization and reduces extrusion. The ossicular prostheses with the head plate specifically designed to cradle the malleus12 can be grouped into three main types: 1. Those with a strut for interposition between the malleus and stapes capitulum (e.g. the Black spanner strut (hydroxyapatite), the Grate strut (Plastipore) and the Kartush strut (hydoxyapatite). 2. Those with a malleus notch extension at the head plate (e.g. the Goldenberg prosthesis (hydroxyapatite) and the Wehrs single or double notch prosthesis (hydroxyapatite).

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Fig. 5  View of a partial ossicular replacement prosthesis from the facial recess in the left ear Ref. Hearing gesults with the Bornhoffer ossicular replacement prostheses. Laryngoscope. 1998 Apr;108:531-6

3. Those with a malleus groove incorporated on the surface of the head plate (e.g. the Dornhoffer prosthesis (hydroxyapatite), the Haberman prosthesis (hydroxyapatite), the Richards design prosthesis (hydroxyapatite) and the Bojrab prosthesis (hydroxyapatite). The titanium ossicular prosthesis was first introduced in 1993. The strength of the material allows the prosthesis to be made with an open head plate and a thin shaft, while preserving sound conduction. The titanium prostheses have a flat, open head plate designed to sit under the tympanic membrane with a groove for the handle of malleus. The open head plate offers visibility of the head of the stapes for accurate placement of the prosthesis into the middle ear and on to the head of malleus. The lower end is bell shaped, which fits easily on to the stapes captitulum providing good contact and excellent sound transmission. The slits in the bell provide space for the stapedius tendon and allow modification of the bell size. The titanium prosthesis with malleus notch was designed by the author13 to combine the benefits of an open head plate and a malleus notch to cradle the malleus.

Advantages of Malleus Notch • The malleus notch could increase the stability of the prosthesis. • A malleus notch extension at the head plate could reduce tilting of the prosthesis. • The size of the head plate of the malleus notch prosthesis was smaller The small head plate would make insertion of the prosthesis easier (Fig. 6).

124  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 6  The malleus notch

Titanium Prosthesis with Malleusnotch for Malleus-stapes Assembly Middle ear implants made of titanium are of two types; fixed and variable length. The length adjustable and malleable tympanoplasty prostheses allows the surgeon to intraoperatively customize for each implant in 0.25 mm increments. The functional length (FL) is measured from the transplant (i.e. cartilage) placed underneath the tympanic membrane, to prevent prosthesis extrusion, to the stapes capitulum in partial reconstruction. The FL is significantly important in partial reconstructions where a very short prosthesis is often demanded. Although hearing outcome is influenced by many factors, tilting of the prosthesis headplate and dislocation from its ideal position with possible total loss of contact to the tympanic membrane are major issues in poor postoperative hearing outcome.11,14 A common clip prosthesis type Dresden (length, 2.5 mm) was modified with a ball joint between prosthesis plate and shaft. The demonstrated intraoperative angle of 60–90° shows the need and the benefit of the integrated microball joint that enables the prosthesis headplate to automatically adjust to the angle and position of the tympanic membrane. Another advantage of the joint design is that large (nonacoustic) movements of the tympanic membrane will not be entirely transmitted to the inner ear. This is because the ball joint will cause the headplate to move and be adjusted depending on the direction of the force applied. Thus, some of the (nonacoustic) force applied is absorbed contrary to a rigid prosthesis that will not be able to adjust its headplate position. Therefore, the new prosthesis is a further step toward the development of a functional middle ear implant that can reproduce both middle ear functions: sound conduction and inner ear protection against atmospheric pressure variations.15

Ossicular Reconstruction 125

Dornhoffer Partial Ossicular Replacement Prosthesis Dornhoffer PORP prosthesis has a hydroxyapatite head and hence can be placed under the tympanic membrane (Fig. 7) also. The shaft is made of titanium and has a fixed length of 2 mm. For placing the prosthesis, when necessary, the malleus handle is oriented by lateral and posterior retraction or by cutting the tensor tympani. The head of the prosthesis can also be bent by 15–30° at its joint with the shaft to fit the contour of the malleus and tympanic membrane. The lower end has a bell shape with slits, which fits over the stapes head. The advantage of the fixed length is that it cuts down the time taken for measurement and prosthesis sizing. The prosthesis is stabilized by the tensor tympani seen to the right, the medial projection of the malleus manubrium to the left, the cartilage graft cap laterally, and the stapes head medially. The bend in the prosthesis at the junction between the shaft and head is to fit the contour of the malleus and tympanic membrane. Superior performance of PORPs compared with TORPs is mainly due to the increased stability afforded by the stapes superstructure when PORPs are used. Earlier in the chapter, we have discussed the reasons of prosthesis failure when TORPs are used and also the two point stabilization technique to improve the results of TORPs. In the design of the Dornhoffer TORP, a large emphasis was placed on the head design of the prosthesis, to incorporate the malleus and to shift the center of gravity over the shaft for increased stability. With these modifications, a more equal comparison between the PORP and TORP is possible, and the importance of the malleus becomes clearer when results are reviewed.16 Worse hearing results occurred when there was severe middle ear fibrosis, even when the stapes was present. In such situations, removal of the superstructure

Fig. 7  View of partial ossisular replacement prosthesis in the left ear

126  Current Concepts of Otitis Media and Recent Management Strategies of stapes with the laser was done to reduce fibrosis. The hearing results in canalwall-down procedure is poor because of a shallow middle ear cleft, which is less acoustically efficient and preservation or reconstruction of the canal wall produces better hearing results, with less chance for contact and fibrosis of the prosthesis to the promontory or facial nerve. Partial mastoid obliteration and reconstruction of the tympanic ring with cartilage, when performing canal down surgery, deepens the middle ear cleft, providing better hearing results.17 Also, the Dornhoffer prosthesis was available in two sizes, 2 mm for the PORP and 4 mm for the TORP. This was an advantage for the surgeon as the time taken to measure and cut the prosthesis was significant.

Ossiculoplasty Techniques Used • Incorporation of the malleus with engagement of the prosthesis at the undersurface of the malleus neck and the proximal portion of the manubrium. In this location, the abnormal position of the malleus handle does not interfere with hearing or stability. • Dornhoffer hydroxyapatite head with titanium shaft ossicular prosthesis (Grace Medical, Memphis, Tennessee, USA) of the same length for every case (2 mm PORP and 4 mm TORP). When necessary, the malleus and/or tympanic membrane orientation were modified to fit these standard prosthesis sizes. • Bending of the head of the prosthesis roughly 15–30° at its joint with the shaft to fit the contour of the malleus manubrium and tympanic membrane. • Should be a free standing reconstruction without use of packing materials. • Placement of a large cartilage graft over the head of the prosthesis (ranging from 30–100% of the surface area of the drumhead). • Use of a Dornhoffer titanium footplate shoe (Grace Medical, Memphis, Tennessee, USA) for cases involving a TORP. • When tympanic membrane repair was required, it was undertaken concurrently with ossiculoplasty as a single stage. A tympanostomy tube was placed in the same sitting, if there was a middle ear effusion intraoperatively (cases with atelectasis but no perforation), if the subject had contralateral active manifestations of eustachian tube dysfunction or if some other underlying condition associated with permanent eustachian tube dysfunction (craniofacial syndrome, radiation exposure, etc.) was present when this standardized technique is adopted, OOPS index seems to be a valid means of predicting hearing outcomes.18

TOTAL OSSICULAR REPLACEMENT PROSTHESIS Defined indentations at the head plate help intraoperatively to indicate the position of the oval shaped stem inferiorly, to position on the oval shaped footplate matchingly. The shaft is made of grade 2 titanium with outstanding malleability. The partially roughened surface improves implant stability on the stapes footplate. A too long prosthesis may stress the ligaments of the stapes footplate and thereby influence sound transmission negatively. The roughened ends stabilizes prosthesis placement. Vlaming and Feenstra19 have demonstrated that prosthesis should be placed along an imaginary line through the center of the footplate and the head of

Ossicular Reconstruction 127

Fig. 8  Side view of a total prosthesis with the silastic band between tympanic membrane and stapes footplate

the stapes. Goode and Nishihara20 have also shown that assemblies are often mechanically inefficient if angulated at an angle greater than 45° from the axis of the superstructure. Technique of silastic banding21 (Fig. 8) allows prosthesis placement in a vertical plane and prevents contact with the promontory, which may impair sound transmission. The tilting motion of the footplate is negligible, regardless of the position of the distal tip of the shaft of the prosthesis on the footplate. In all cases in our series, the band allowed a proper prosthesis placement, particularly because the distal end of the prosthesis was always centered on the footplate. According to Vlaming and Feenstra this configuration achieves an almost perpendicular direction of the forces to the foot plate with optimal transfer function and minimal dissipation of energy. With this technique the prosthesis is firmly attached to the stapes, thus decreasing the risk of displacement of the prosthesis despite the absence of the malleus.

Kurz Connector Achieving a stable position of TORP is demanding because of a limited view on the TORP footplate interface and individual angles between the footplate and tympanic membrane. Prosthesis with a microball shaped handle is flexible and also adjusts for the various alignments of the foot plate and tympanic membrane or malleus.

Extensible Prosthesis (TORP and PORP) (Figs 9 and 10) Malleable titanium implant with an adjustable stem, extensible implant body can lengthened or shortened while in the operative site.

128  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 9  Invotec extensible prosthesis (PORP)

Fig. 10  Invotec extensible prosthesis

Ossicular Reconstruction 129

A

B

Figs 11A and B  Vincent’s malleus replacement prosthesis

Absence of the malleus handle can affect hearing results after ossiculoplasty. To enhance middle ear prosthesis stability, recreation of malleus handle can be important. In close conjunction with Robert Vincent MD from Beziers, France (Causse Ear Clinic), KURZ has developed a new concept of tympanoplasty. The malleus replacement prosthesis (MRP) (Figs 11A and B) is implanted underneath the tympanic membrane at any position in the external ear canal. It is attached via a Y-shaped titanium wire with two hooks. The surgeon inserts the MRP and connects any partial or total replacement prosthesis due to the malleable MRP. The neo malleus should be kept in proper position during the initial healing period, to reduce the risk of tilting.

REFERENCES 1. Committee on Hearing and Equilibrium guidelines for the evaluation of results of treatment of conductive hearing loss. American Academy of Otolaryngology-Head and Neck Surgery Foundation, Inc. Otolaryngol Head Neck Surg. 1995;113(3):186-7. 2. Martin AD, Harner SG. Ossicular reconstruction with titanium prosthesis. Laryngoscope. 2004;114(1):61-4. 3. Stupp CH, Dalchow C, Grun D, et al. Three years of experience with titanium implants in the middle ear. Laryngorhinootologie. 1999;78(6):299-303. 4. Merchant SN, McKenna MJ, Rosowski JJ. Current status and future challenges of tympanoplasty. Eur Arch Otorhinolaryngol. 1998;255(5):221-8. 5. Merchant SN, Ravicz ME, Voss SE, et al. Toynbee memorial lecture 1947. Middle ear mechanics in normal, diseased and reconstructed ears. J Laryngol Otol. 1998;112(8):715-31. 6. Maassen MM, Löwenheim H, Pfister M, et al. Surgical-handling properties of the titanium prosthesis in ossiculoplasty. Ear Nose Throat J. 2005;84(3):142-4, 147-9. 7. Neff BA, Rizer FM, Schuring AG, et al. Tympano-ossiculoplasty utilizing the spiggle and theis titanium total ossicular replacement prosthesis. Laryngoscope. 2003;113(9):1525-9. 8. Zenner HP, Stegmaier A, Lehner R, et al. Open Tubingen titanium prostheses for ossiculoplasty: a prospective clinical trial. Otol Neurotol. 2001;22(5):582-9.

130  Current Concepts of Otitis Media and Recent Management Strategies 9. Krueger WW, Feghali JG, Shelton C, et al. Preliminary ossiculoplasty results using the Kurz titanium prostheses. Otol Neurotol. 2002;23(6):836-9. 10. Bared A, Angeli SI. Malleus handle: determinant of success in ossiculoplasty. Am J Otolaryngol. 2010;31(4):235-40. 11. De Vos C, Gersdorff M, Gerard JM. Prognostic factors in ossiculoplasty. Otol Neurotol. 2007;28(1):61-7. 12. Smith & Nephew. The Catalog. USA: Smith & Nephew,1999. 13. Yung M. Titanium prosthesis with malleus notch: a study of its ‘user-friendliness’. J Laryngol Otol. 2007;121(10):938-42. 14. Yung M, Vowler SL. Long-term results in ossiculoplasty: an analysis of prognostic factors. Otol Neurotol. 2006;27(6):874-81. 15. Beutner D, Luers JC, Bornitz M, et al. Titanium clip ball joint: a partial ossicular reconstruction prosthesis. Otol Neurotol. 2011;32(4):646-9. 16. Dornhoffer JL, Gardner E. Prognostic factors in ossiculoplasty: a statistical staging system. Otol Neurotol. 2001;22(3):299-304. 17. Dornhoffer JL. Surgical modification of the difficult mastoid cavity. Otolaryngol Head Neck Surg. 1999;120(3):361-7. 18. Gluth MB, Moore PC, Dornhoffer JL. Method and reproducibility of a standardized ossiculoplasty technique. Otol Neurotol. 2012;33(7):1207-12. 19. Vlaming MS, Feenstra L. Studies on the mechanics of the reconstructed human middle ear. Clin Otolaryngol Allied Sci. 1986;11(6):411-22. 20. Goode RL, Nishihara S. Experimental models of ossiculoplasty. Otolaryngol Clin North Am. 1994;27(4):663-75. 21. Vincent R, Sperling NM, Oates J, et al. Ossiculoplasty with intact stapes and absent malleus: the silastic banding technique. Otol Neurotol. 2005;26(5):846-52.

21

Hearing Aids Swapna Sabastian, L Paul Emerson

INTRODUCTION Hearing aids (HAs) may be necessary in chronic otitis media (COM) to restore hearing. In eosinophilic otitis media (EOM) there could be associated sensorineural (SN) loss. Hearing restoration may be unsuccessful in recurrent EOM. Patients may develop SN loss also following surgery. Use of ototoxic eardrops, presence of tympanosclerosis, and failure of surgery for COM are other factors for HA use. At times due to persistent mucosal disease, ear discharge may continue and bone conduction, HAs may need to be fitted. Also, patient’s medical condition and age may not at times allow surgical restoration of hearing to be considered. Hearing aids are amplifying devices. The concept of HA came from the use of cupped hand behind the ear (BTE). This produces 5–10 dB of gain at mid and high frequencies. The earlier HAs were in the shape of trumpet, horn or funnel. This was followed by carbon HAs, which used carbon microphone and vacuum tube HAs. Use of transistors and integrated circuits reduced the size of the HAs.1,2 The components of a HA are a microphone to convert sound into electricity, an amplifier to increase the strength of the electrical signal, a miniature loudspeaker called the receiver to turn electricity back into sound, a battery to provide the power needed by the amplifier.

INDICATIONS Hearing aids are indicated in COM patients as an adjunct to surgery, or in severe disease with nonreconstructable middle ear, or when elderly patients prefer HA to surgery.

TYPES OF HEARING AIDS (Figs 1A and B) Depending on where they are worn HAs can be classified as: • Body worn • Spectacle type • Behind the ear type • In the ear • In the canal • Completely-in-the-canal (CIC).

132  Current Concepts of Otitis Media and Recent Management Strategies

Fig. 1A (Source: http://www.digitalhearing.com.au/upload/HearingAids_oticon.jpg)

Hearing Aids 133

Fig. 1B Figs 1A and B  Hearing aids

Body Worn Body worn HAs, as the name implies is worn on the body either in a pocket, pouch or on the belt. They are connected via a cable containing wires to a receiver. The receiver can plug into an earmold, which is custom made for the individual’s ear canal and concha.

Behind the Ear The behind the ear aids sits behind the ear. The microphone, amplifier and receiver are mounted inside the banana-shaped case and the sound is conveyed acoustically via a tube to a custom earmold.

In the Ear In the ear HAs can vary in size from full concha style, which fills the entire concha to about half shell, which fills only the lower half of the concha.

In the Canal In the canal HA occupies only a small portion of the concha.

134  Current Concepts of Otitis Media and Recent Management Strategies

Completely-in-the-canal Completely-in-the-canal HAs fit entirely within the ear canal. A nylon thread with a small knob on the end is attached to the HA that extends into the concha, which helps in removing these HAs from the ear. Peritympanic CIC HAs are the ones whose medial end is within a few millimeters of the eardrum. In the spectacle model, the part that fits BTE is sawn off and a short adapter is glued on in its place. The HA components are attached to this adapter and a tube leads from the adapter to the ear. Hearing aids can be analog or digital. Analog hearing instruments amplify the soundwave using transistors in a circuit. Any changes to the sound of the HA are made with the volume control or small trimmers to adjust the response.

DIGITAL HEARING AID A digital HA or digital signal processor (DSP) takes the incoming signal from the microphone, converts it into a digital format, and then processes the signal using digital technology before converting it back into an analog sound to be delivered to the ear. Digital HAs have advanced signal processing schemes. For example, digital technology helps in determining, which signals are most speech like and which sounds are most likely noise and then program the aid to essentially amplify the speech like sounds, while trying to reduce the background noises. This gives better comfortable listening experience.3 In hearing aids, acoustic feedback occurs when some of the amplified sound leaks from the ear canal, and is picked up by the HA microphone and then reamplified, which results in a disturbingly loud tonal signal. The method of reducing acoustic feedback in an analog HA has been to increase the acoustic seal in the ear canal, by using tight earmolds. But for people with the most severe hearing losses, they are often unable to achieve the desired amplification targets because of the occurrence of acoustic feedback, no matter how well fit the earmold is. Adaptive feedback cancellation algorithms are techniques that are used to implement a neutralizing electronic feedback path that suppresses the tonal feedback signal in digital HAs. Feedback cancellation circuits (FBC) continually monitor the output of the HA to determine whether some portion of the amplified signal contains elements that have the acoustic characteristics of acoustic feedback. When it does, the feedback circuit first determines the frequency, amplitude and phase of the feedback component and then generates signals of opposite phase that will cancel (or markedly reduce) the feedback component. Incorporation of digital control circuits and digital memories to the HAs enabled the amplification characteristics of HAs to be adjusted or programmed by the clinician.4 The user can change from one program to another depending on the hearing needs in multi memory digitally programmable HA.

BONE CONDUCTION RETAIN HEARING AID For those who cannot use the regular type of HAs coupled to the ear canal due to various reasons such as chronic inflammation of the external canal or middle ear, or bone disease, or who have congenital malformations of the pinna, external auditory canal or middle ear, and bone conduction HAs are used.5,6

Hearing Aids 135 Bone conduction HAs directly vibrate the skull, which in turn transmits these vibrations to the cochlea. Bone conduction HAs are of two types: 1. Traditional bone conduction HA. 2. Bone anchored hearing aid (BAHA).

Traditional Bone Conduction Hearing Aid A traditional bone conduction HA, consists of a body-worn aid and bone conductor or vibrator fitted to a head band. The head band holds the vibrating part tightly to the head, close to the mastoid process. It is also possible to fit the bone conductor to the arm of a pair of specially strengthened spectacles instead of a headband or with a BTE HA attached to the headband.

Bone Anchored Hearing Aid (Fig. 2) The bone-anchored hearing aid consists of a permanent titanium implant, which is surgically inserted into the part of the skull bone that is BTE. It has a detachable external sound processor with directional microphone. BAHA requires the patient to have a titanium screw permanently protruding from the skull through the skin, to which the external device itself is attached.7 The BAHA consists of three parts: 1. The titanium implanted portion. 2. An external abutment. 3. The sound processor that clips onto the abutment. The system functions by transmitting sound to the inner ear through the bone bypassing the ear canal and the middle ear. The titanium implant is placed during a minor surgical procedure and over time integrates with the bone BTE. The hearing device transmits sound vibrations through the titanium implant to the skull and the inner ear. BAHA do not have the approval of the United States (US) Food and Drug Administration (FDA) for use in children less than 5 years of age.

Fig. 2  Bone anchored hearing aid (BAHA) (Source: http://laboratoire.pontet.net/details-appareils+auditifs+conduction+osseuse+le+b aha-259.html)

136  Current Concepts of Otitis Media and Recent Management Strategies Having a bone disease that leaves the skull too thin to support a BAHA implant like brittle bone disease (osteogenesis imperfecta) is another contraindication for BAHA.

IMPLANTABLE HEARING AID (Figs 3A and B) Patients with moderate-to-severe hearing loss are good candidates for conventional HAs. Sometimes it may not be possible to use conventional HAs for

A

B Figs 3A and B  Middle ear implant (Source: Maurer J, Savvas E. The Esteem System: a totally implantable hearing device. Adv Otorhinolaryngol. 2010;69:59-71.)

Hearing Aids 137 medical reasons such as recurrent otitis externa or malformation of the external ear. Middle ear implants have been developed as a treatment option for those patients who are either unable to wear or are dissatisfied with conventional HAs. The first fully implantable middle ear device was developed in 1999 and marketed as the totally integrated cochlear amplifier.8 However, it was withdrawn from the market in 2001 because of technical and economic problems. Two fully implantable middle ear devices are currently available for use: 1. The Esteem hearing system. 2. The Carina fully implantable hearing device.9 The Esteem system has been marketed in Europe since 2006 and obtained US FDA approval in 2010. The Esteem device consists of three components are: 1. A sound processor. 2. Two piezoelectric transducers called the driver. 3. The sensor. The sensor is placed on the incus where it detects tympanic membrane motion, converts it to an electrical signal, and sends it to the sound processor. The signal is then sent to the ‘driver’, which causes vibration of the stapes.10 To prevent feedback from the device, implantation requires separation of the incudostapedial joint and resection of a segment of the long process of the incus. Therefore, if the device fails or must be removed, the incus needs to be replaced with a prosthesis to recreate the ossicular chain.11 The expected battery life is 4½ years with continuous usage (24 h/day, 7 day/week) to 9 years (if only used for 8 h/day).12 When it requires changing, it can be done as an outpatient surgical procedure under local anesthesia. The manufacturer’s website provides an estimated cost of $30,000 for the device.13 The first reported implantation of the Carina device occurred in France in 2005, but the device is yet to be approved for use in the US. The current device is fully implantable. Sounds are picked up by a subcutaneous, retroauricular microphone, amplified and converted into an electrical signal that is, in turn, relayed to a transducer attached to the incus. The transducer then translates electrical signals into a mechanical motion that directly stimulates the ossicular chain. To charge the battery, a charging coil is placed on the skin over the implant. The charger can be worn on a belt or waistband. The charging time is about 1–1½ hours.14 Complications were most commonly taste disturbance. Device failure was common with the Carina, predominately related to charging difficulties. For both devices, there were clinically significant improvements in functional gain, speech reception and speech recognition over the unaided conditions. In studies comparing the Esteem or Carina to HAs, findings were mixed. Although improvements in functional gain were similar to those for HAs, speech recognition and quality of life were greater with the implants. Despite limited evidence, these devices seem to offer a relatively safe and effective treatment option, particularly for patients who are medically unable to wear conventional HAs.

BONE CONDUCTION IMPLANTABLE HEARING AIDS Bone conduction implantable (BCI) HAs can be used to bypass defective middle ear, transmitting sounds to the inner ear by sending vibrations right through the skull bone. The implant is attached BTE, under the skin, directly into the surface

138  Current Concepts of Otitis Media and Recent Management Strategies of the skull. It is paired with an external sound processor, which actually receives sounds from the outside world. An induction coil in the implant allows it to receive sound transmitted through the skin from the processor. The implant then uses a quadratic loudspeaker to relay those sound vibrations into the bone of the skull, through which they travel to the inner ear. The processor can simply be pulled off when not needed. These devices have not been used in children.

BILATERAL AMPLIFICATION Bilateral hearing is necessary for localization and for best performance in noise.15-17 Auditory deprivation has been documented in children fitted with unilateral amplification.18,19 Therefore, in children with bilateral hearing loss, it is recommended that unless contraindicated should be fitted with bilateral amplification. For patients with severe to profound unilateral hearing loss (or very poor word recognition unilaterally), contralateral routing of signal (CROS) system may be considered. In CROS HA system, the transmitter placed behind or inside the poorer ear, picks up sound and transmits it wirelessly to the normal hearing ear. The hearing in the good ear will remain natural and completely unaffected.20 For patients with severe to profound hearing loss (or very poor word recognition) in one ear and an aidable hearing loss in the other ear, a bilateral CROS (BiCROS) system may be considered. The transmitter placed behind or inside the poorer ear, picks up sound and transmits it wirelessly to the better hearing ear. At the same time, the receiving HA also serves as an amplifier improving hearing in the better ear. An infant or young child should be seen by an audiologist every 3 months during the first 2 years of using amplification and every 6 months after that for behavioral audiometric evaluations, current assessment of communication abilities, needs and demands, adjustment of the amplification system based on updated audiometric information and communication demands, periodic electroacoustic evaluations, earmold fit check, etc.21-23

COCHLEAR IMPLANT Patients with severe to profound SN hearing loss in both ears with no benefit from HAs are cochlear implant candidates. Cochlear implants provide the perception of sound through the conversion of sound stimuli into electrical impulses, which are received by the cochlear nerve and processed by the central auditory system. Cochlear implant consists of external parts, which include a microphone, a speech processor and a transmitter. The microphone picks up sounds and sends them to the speech processor and surgically implanted parts that work together to allow the user to perceive sound. The speech processor is a computer that analyzes and digitizes the sound signals and sends them to a transmitter worn on the head just BTE. The transmitter sends the coded signals to an implanted receiver just under the skin. The internal (implanted) parts include a receiver and electrodes. The receiver is just under the skin BTE. The receiver takes the coded electrical signals from the transmitter and delivers them to the array of electrodes that have been surgically inserted in the cochlea. The electrodes stimulate the fibers of the auditory nerve and sound sensations are perceived.

Hearing Aids 139

CONCLUSION Sometimes HA is necessary to improve hearing in patients with COM. Today, there is a variety of HAs available depending on the hearing loss as well as cost factors and cosmesis.

REFERENCES 1. Lybarger SF. A historical overview. In: Sandlin RE (Ed). Handbook of Hearing Aid Amplification. Boston: College Hill Press; 1998. pp. 1-29. 2. Berger K. The hearing aid—its operation and development. Livonia, MI: National Hearing Aid Society. 1984. 3. Levitt H. Digital hearing aids: a tutorial review. J Rehabil Res Dev. 1987;24(4):7-20. 4. Levitt H. Digital hearing aids: past, present and future. In: Tobin H (Ed). Practical Hearing Aid Selection and Fitting (Monograph 001 xi-xxiii). Washington DC: Dept of Veterans Affairs 1997. 5. Snik AF, Mylanus EA, Cremers CW. The bone-anchored hearing aid: a solution for previously unresolved otologic problems. Otolaryngol Clin North Am. 2001;34(2):365-72. 6. Tjellstrom A, Hakansson B, Granstrom G. Bone anchored hearing aids: current status in adults and children. Otolaryngol Clin North Am. 2001;34(2):337-64. 7. Tjellstrom A, Håkansson B. The bone anchored hearing aid. Design principles, indications, and long term clinical results. Otolaryngology Clin North Am. 1995;28(1):53-72. 8. Siegert R, Mattheis S, Kasic J. Fully implantable hearing aids in patients with congenital auricular atresia. Laryngoscope. 2007;117(2):336-40. 9. Zenner HP, Rodriguez JJ. Totally implantable active middle ear implants: ten years’ experience at the University of Tubingen. Adv Otorhinolaryngol. 2010;69:72-84. 10. Maurer J, Savvas E. The Esteem System: a totally implantable hearing device. Adv Otorhinolaryngol. 2010;69:59-71. 11. Yu KC, Cheung SW. General considerations of implantable middle ear hearing devices. Current Diagnosis and Treatment in Otolaryngology. New York, NY: McGraw Hill-Access Medicine; 2010. 12. Esteem(R) Battery Longevity. Saint Paul, MN: Envoy Medical Corporation, 2012 (Online). Available from www.envoymedical.com/batteryreplacement. [Accessed January 15, 2012] 13. Cost of the Esteem. Saint Paul (MN): Envoy Medical Corporation; 2010 (Online). Available from www.envoymedical.com/cost-of-the-esteem. (Accessed January 15, 2012) 14. Kirkwood D. Middle ear implants offer potential: new breed of devices may stimulate compliance, experts say. ENT Today, 2011; 8. [Online] Available from http://www. enttoday.org/details/article/1057637/MiddleEarImplants Offer Potential New breed of devices may stimulate complianc.html. [Accessed November 2013]. 15. Hawkins DB, Yacullo W. Signal-to-noise ratio advantage of binaural hearing aids and directional microphones under different levels of reverberation. J Speech Hear Disord. 1984;49(3):278-86. 16. Valente M. Binaural amplification: Part 1. Audiol. J for Continuing Education 1982a;7(6). 17. Valente M. Binaural amplification: Part 2. Audiol. J for Continuing Education. 1982b;7(6). 18. Boothroyd A. Recovery of speech perception performance after prolonged auditory deprivation: case study. J Am Acad Audiol. 1993;4(5):331-6.

140  Current Concepts of Otitis Media and Recent Management Strategies 19. Hattori H. Ear dominance for nonsense-syllable recognition ability in sensorineural hearing-impaired children: Monaural versus Binaural amplification. J Am Acad Audiol. 1993;4(5):319-30. 20. Harford E, Barry J. A rehabilitative approach to the problem of unilateral hearing impairment: Contralateral routing of signals (CROS). J Speech Hear Disord. 1965;30:121-38. 21. Bess FH, Dodd-Murphy J, Parker RA. Children with minimal sensorineural hearing loss: prevalence, educational performance, and functional status. Ear Hear. 1998;19(5):339-54. 22. Bess FH, Tharpe AM. Unilateral hearing impairment in children. Pediatrics. 1984;74:206-16. 23. Matkin ND. The potential benefits of amplification for young children with normal hearing In: Bess FH, Gravel JS, Tharpe AM (Eds). Amplification for Children with Auditory Deficits. Nashville: Bill Wilkerson Center Press; 1996.

Index Page numbers followed by f refer to figure and t refer to table.

A Adrenaline 85 Allergy, management of 64 Antibiotics 49 Aspergillus fumigatus 54 Atopic disease 61 Austin-Kartush ossicular classification 78f

B Bacterial resistance 49 Basal cells 55 Bellucci classification 77, 79t Biofilm development cycle 39f Bony annulus, level of 111f Bupivacaine 85

C Canaloplasty 89 Candida albicans 54 Cartilage tympanoplasty, classification of 110 Central nervous system 86 Chlamydia pneumoniae 51 Chlamydophila pneumoniae 66 Chorda tympani 94 Chronic tympanostomy tube otorrhea 40 Churg-Strauss syndrome 73 Cochlear implant 138 Computed tomography scan 20, 48, 73

Dornhoffer partial ossicular replacement prosthesis 125 Duesseldorf titanium prosthesis 118f Dust mite 64

E Endaural incision 91f Epinephrine 85 Epitympanum, anterior 55 Erythrocyte sedimentation rate 60 Eustachian tube 6f, 10, 11f, 12f, 14, 16f, 20, 21, 22f, 30 dysfunction 17 function 10, 17, 18 obstruction 13 opening of 22f patency 50 physiology of 13, 14f role of 10 Eustachian tuboplasty 26

F Facial nerve 6f, 7f, 8

G Gastroesophageal reflux disease 24 Gastrointestinal tract 65 Goblet cells 12 Granulation tissue 49

D

H

Dihydroxyphenyl methylaminoethanol 85 Dilatory dysfunction 24 Dornhoffer cartilage mosaic tympanoplasty 113 Dornhoffer graft 115f Dornhoffer hapex total ossicular replacement prosthesis 79

31, 36, 51, 65, 70 Harvesting graft 89 Hearing aid 131, 133f bone anchored 135, 135f bone conduction implantable 137 digital 134 implantable 136

142  Current Concepts of Otitis Media and Recent Management Strategies traditional bone conduction 135 types of 131 Human immunodeficiency virus 33 Hydraulic lever 9 Hydroxyapatite 119 Hypereosinophilic syndrome 73 Hypotympanum 55

I Incision 89 Incus 4, 122 Intact canal wall 82

J Jigsaw technique 113 Jugular bulb 6f

K Klebsiella pneumoniae 53 Kurz connector 127

L Laryngopharyngeal reflux 24 Leukotrienes 59 Levator veli palatini 10, 16, 22f Lidocaine 84-86 Lignocaine 84

M Magnetic resonance imaging 73 Malleus 3 head fixation 108 notch 123, 124f Marcaine 85 Mast cells 57 Mastoidectomy 82 Mastoiditis, acute 38f Membrane cofactor protein 57 Mild infection 32 Moraxella catarrhalis 31, 36, 51, 66 Mucosa associated lymphoid tissue 13 Mucosal damage 31 disease 10, 47 Mycoplasma pneumoniae 66 Myringoplasty 88, 103 Myringotomy 33

O Ossicular reconstruction 117 Ossiculoplasty outcome parameters staging index 80f Otitis media 29, 36, 41, 56, 59, 73 acute 20, 29-33, 33t, 39, 51, 55, 57, 59, 69 chronic 10, 25, 29, 32, 36, 46, 47, 53, 55-57, 59, 72, 131 eosinophilic 72, 75, 131

P Palisades technique 110 Partial ossicular replacement prosthesis 79, 119 Patulus disease 26 Plastipore 119 Platelet-activating factor 59 Pneumococcal conjugate vaccine 69 Pneumococcal disease 69, 70 Pneumococcal vaccination 69 Politzer test 19 PORP reconstruction 122 Posterior canal incision 91f Posterior sinus 7 Post-tympanostomy tube otorrhea, classification of 39 Pressure equalizing tube 62f Pressure regulation function 16, 16f Prostaglandins 59 Prosthesis angular clip 122f extensible 127 total ossicular replacement 117, 126 Prosthetic material, choice of 119 Pseudomonas aeruginosa 40, 47, 53 Pyramidal eminence 6f, 7f

R Reconstructed canal wall 82 Recurrent tympanostomy tube otorrhea, prevention of 40 Resistant infection 32 Respiratory infection, recurrent 60 Respiratory syncytial virus 66 Retractors, placement of 93f Retroauricular periosteal flap 95f

Index 143 Retrotympanum 5 endoscopic anatomy of 7f parts of 6f Rhinosinusitis 24

S Sclerosis, fibrocystic and fibro-osseous 46 Secretory cells 55 Signal system, contralateral routing of 138 Sinus tympani 5f, 7f Sonotubometry 19 Spiral flap technique 96f Staphylococcus aureus 33, 40, 47, 53 Steroid-containing drops 49 Streptococcus pneumoniae 31, 36, 37f, 40, 51, 65, 69 Streptococcus pyogenes 51

T Temporalis fascia 89, 89f, 95f graft, excision of 90f Tensor tympani 10 Tensor veli palatine, location of 22f Tensor veli palatini muscle 10, 16 contraction of 16f Titanium prosthesis 124 Toynbee test 19

Tubal lumen, mucous membrane of 11 Tubal-opening mechanism 16 Tympanic membrane 1, 3, 18, 33f, 47, 55, 81, 103, 110 Tympanometry 19 Tympanoplasty 82, 83, 88, 103, 104, 105f, 106f, 107, 108f, 109f, 114 classification of 81, 82 surgery of 103 Tympanostomy tube otorrhea, prevention of 39

U Upper respiratory infection 30, 59

V Vaccine schedule 70 Valsalva maneuver 17 Valsalva test 18 Ventilation tubes 33 Vincent’s malleus replacement prosthesis 129f Viscosity 49

W White blood cell 66 Wullstein’s classification 82